1
40
14
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/sctm.17-0046" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/sctm.17-0046</a>
Pages
1759–1766
Issue
9
Volume
6
Dublin Core
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Title
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A Novel Role for CAMKK1 in the Regulation of the Mesenchymal Stem Cell Secretome.
Publisher
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Stem cells translational medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-09
Subject
The topic of the resource
Calcium/calmodulin-dependent protein kinase kinase-1; Cardiac disease; Cardiac regeneration; Mesenchymal stem cells; Secretome
Creator
An entity primarily responsible for making the resource
Dong Feng; Patnaik Shyam; Duan Zhong-Hui; Kiedrowski Matthew; Penn Marc S; Mayorga Maritza E
Description
An account of the resource
Transplantation of adult stem cells into myocardial tissue after acute myocardial infarction (AMI), has been shown to improve tissue recovery and prevent progression to ischemic cardiomyopathy. Studies suggest that the effects of mesenchymal stem cells (MSC) are due to paracrine factors released by MSC, as the benefits of MSC can be achieved through delivery of conditioned media (CM) alone. We previously demonstrated that downregulation of Dab2 enhances MSC cardiac protein expression and improves cardiac function after AMI following MSC engraftment. In order to define the molecular mechanisms that regulate MSC secretome, we analyzed gene arrays in MSC following downregulation of Dab2 via TGFbeta1 pretreatment or transfection with Dab2:siRNA or miR-145. We identified 23 genes whose expressions were significantly changed in all three conditions. Among these genes, we have initially focused our validation and functional work on calcium/calmodulin-dependent protein kinase kinase-1 (CAMKK1). We quantified the effects of CAMKK1 overexpression in MSC following injection of CM after AMI. Injections of CM from MSC with CAMKK1 over-expression correlated with an increase in vascular density (CAMKK1 CM: 2,794.95 +/- 44.2 versus Control: 1,290.69 +/- 2.8 vessels/mm(2) ) and decreased scar formation (CAMKK1 CM 50% +/- 3.2% versus Control: 28% +/- 1.4%), as well as improved cardiac function. Direct overexpression of CAMKK1 in infarcted tissue using a CAMKK1-encoding plasmid significantly improved ejection fraction (CAMKK1: 83.2% +/- 5.4% versus saline: 51.7% +/- 5.8%. Baseline: 91.3% +/- 4.3%) and decreased infarct size after AMI. Our data identify a novel role for CAMKK1 as regulator of the MSC secretome and demonstrate that direct overexpression of CAMKK1 in infarcted cardiac tissue, results in therapeutic beneficial effects. Stem Cells Translational Medicine 2017;6:1759-1766.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/sctm.17-0046" target="_blank" rel="noreferrer noopener">10.1002/sctm.17-0046</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Calcium/calmodulin-dependent protein kinase kinase-1
Cardiac disease
Cardiac regeneration
Department of Integrative Medical Sciences
Dong Feng
Duan Zhong-Hui
Kiedrowski Matthew
Mayorga Maritza E
Mesenchymal stem cells
NEOMED College of Medicine
Patnaik Shyam
Penn Marc S
Secretome
Stem cells translational medicine
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/CIRCRESAHA.111.300440" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.111.300440</a>
Pages
816–825
Issue
5
Volume
112
Dublin Core
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Title
A name given to the resource
An open-label dose escalation study to evaluate the safety of administration of nonviral stromal cell-derived factor-1 plasmid to treat symptomatic ischemic heart failure.
Publisher
An entity responsible for making the resource available
Circulation research
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
2013-03
Subject
The topic of the resource
*Plasmids; Aged; Brain/blood; Chemokine CXCL12/*genetics/metabolism; Cohort Studies; Dose-Response Relationship; Drug; Echocardiography; Exercise Tolerance; Female; Follow-Up Studies; Genetic Therapy/*adverse effects/*methods; Heart Failure/metabolism/pathology/*therapy; Humans; Male; Middle Aged; Myocardium/metabolism/pathology; Natriuretic Peptide; Peptide Fragments/blood; Positron-Emission Tomography; Quality of Life; Treatment Outcome
Creator
An entity primarily responsible for making the resource
Penn Marc S; Mendelsohn Farrell O; Schaer Gary L; Sherman Warren; Farr Maryjane; Pastore Joseph; Rouy Didier; Clemens Ruth; Aras Rahul; Losordo Douglas W
Description
An account of the resource
RATIONALE: Preclinical studies indicate that adult stem cells induce tissue repair by activating endogenous stem cells through the stromal cell-derived factor-1:chemokine receptor type 4 axis. JVS-100 is a DNA plasmid encoding human stromal cell-derived factor-1. OBJECTIVE: We tested in a phase 1, open-label, dose-escalation study with 12 months of follow-up in subjects with ischemic cardiomyopathy to see if JVS-100 improves clinical parameters. METHODS AND RESULTS: Seventeen subjects with ischemic cardiomyopathy, New York Heart Association class III heart failure, with an ejection fraction
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.111.300440" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.111.300440</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Plasmids
2013
Aged
Aras Rahul
Brain/blood
Chemokine CXCL12/*genetics/metabolism
Circulation research
Clemens Ruth
Cohort Studies
Dose-Response Relationship
Drug
Echocardiography
Exercise Tolerance
Farr Maryjane
Female
Follow-Up Studies
Genetic Therapy/*adverse effects/*methods
Heart Failure/metabolism/pathology/*therapy
Humans
Losordo Douglas W
Male
Mendelsohn Farrell O
Middle Aged
Myocardium/metabolism/pathology
Natriuretic Peptide
Pastore Joseph
Penn Marc S
Peptide Fragments/blood
Positron-Emission Tomography
Quality of Life
Rouy Didier
Schaer Gary L
Sherman Warren
Treatment Outcome
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.3945/jn.113.184291" target="_blank" rel="noreferrer noopener">http://doi.org/10.3945/jn.113.184291</a>
Pages
1030–1036
Issue
7
Volume
144
Dublin Core
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Title
A name given to the resource
Apolipoprotein A1 regulates coenzyme Q10 absorption, mitochondrial function, and infarct size in a mouse model of myocardial infarction.
Publisher
An entity responsible for making the resource available
The Journal of nutrition
Date
A point or period of time associated with an event in the lifecycle of the resource
2014
2014-07
Subject
The topic of the resource
Male; Animals; Mice; Myocardium; Lipid Metabolism; Mitochondria; Heart/drug effects; Antioxidants/administration & dosage/*metabolism/pharmacokinetics/therapeutic use; Apolipoprotein A-I/blood/genetics/*metabolism; Cardiotonic Agents/administration & dosage/metabolism/pharmacokinetics/therapeutic use; Dietary Supplements; Electron Transport Complex II/chemistry/metabolism; Electron Transport Complex III/chemistry/metabolism; Electron Transport/drug effects; Hypoalphalipoproteinemias/physiopathology; Intestinal Absorption; Myocardial Infarction/etiology/metabolism/pathology/*therapy; Myocardial Reperfusion Injury/blood/metabolism/pathology/prevention & control; Myocardium/enzymology/*metabolism/pathology; Tissue Distribution; Ubiquinone/administration & dosage/*analogs & derivatives/metabolism/pharmacokinetics/therapeutic use; Injections; Biological; Models; Animal; Knockout; Intraperitoneal; *Disease Models; Heart/drug effects/enzymology/*metabolism; Proteins; Animal Studies; Apolipoproteins; Coenzyme Q; Proteins – Metabolism; Heart – Drug Effects; Myocardial Infarction – Therapy; Apolipoproteins – Blood; Apolipoproteins – Metabolism; Antioxidants – Administration and Dosage; Antioxidants – Metabolism; Antioxidants – Pharmacokinetics; Antioxidants – Therapeutic Use; Cardiotonic Agents – Administration and Dosage; Cardiotonic Agents – Metabolism; Cardiotonic Agents – Pharmacokinetics; Cardiotonic Agents – Therapeutic Use; Coenzyme Q – Administration and Dosage; Coenzyme Q – Metabolism; Coenzyme Q – Pharmacokinetics; Coenzyme Q – Therapeutic Use; Electron Transport – Drug Effects; Inborn Errors – Physiopathology; Mitochondria – Drug Effects; Mitochondria – Metabolism; Myocardial Infarction – Etiology; Myocardial Infarction – Metabolism; Myocardial Infarction – Pathology; Myocardial Reperfusion Injury – Blood; Myocardial Reperfusion Injury – Metabolism; Myocardial Reperfusion Injury – Pathology; Myocardial Reperfusion Injury – Prevention and Control; Myocardium – Metabolism; Myocardium – Pathology
Creator
An entity primarily responsible for making the resource
Dadabayev Alisher R; Yin Guotian; Latchoumycandane Calivarathan; McIntyre Thomas M; Lesnefsky Edward J; Penn Marc S
Description
An account of the resource
HDL and apolipoprotein A1 (apoA1) concentrations inversely correlate with risk of death from ischemic heart disease; however, the role of apoA1 in the myocardial response to ischemia has not been well defined. To test whether apoA1, the primary HDL apolipoprotein, has an acute anti-inflammatory role in ischemic heart disease, we induced myocardial infarction via direct left anterior descending coronary artery ligation in apoA1 null (apoA1(-/-)) and apoA1 heterozygous (apoA1(+/-)) mice. We observed that apoA1(+/-) and apoA1(-/-) mice had a 52% and 125% increase in infarct size as a percentage of area at risk, respectively, compared with wild-type (WT) C57BL/6 mice. Mitochondrial oxidation contributes to tissue damage in ischemia-reperfusion injury. A substantial defect was present at baseline in the electron transport chain of cardiac myocytes from apoA1(-/-) mice localized to the coenzyme Q (CoQ) pool with impaired electron transfer (67% decrease) from complex II to complex III. Administration of coenzyme Q10 (CoQ10) to apoA1 null mice normalized the cardiac mitochondrial CoQ pool and reduced infarct size to that observed in WT mice. CoQ10 administration did not significantly alter infarct size in WT mice. These data identify CoQ pool content leading to impaired mitochondrial function as major contributors to infarct size in the setting of low HDL/apoA1. These data suggest a previously unappreciated mechanism for myocardial stunning, cardiac dysfunction, and muscle pain associated with low HDL and low apoA1 concentrations that can be corrected by CoQ10 supplementation and suggest populations of patients that may benefit particularly from CoQ10 supplementation.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.3945/jn.113.184291" target="_blank" rel="noreferrer noopener">10.3945/jn.113.184291</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Disease Models
2014
Animal
Animal Studies
Animals
Antioxidants – Administration and Dosage
Antioxidants – Metabolism
Antioxidants – Pharmacokinetics
Antioxidants – Therapeutic Use
Antioxidants/administration & dosage/*metabolism/pharmacokinetics/therapeutic use
Apolipoprotein A-I/blood/genetics/*metabolism
Apolipoproteins
Apolipoproteins – Blood
Apolipoproteins – Metabolism
Biological
Cardiotonic Agents – Administration and Dosage
Cardiotonic Agents – Metabolism
Cardiotonic Agents – Pharmacokinetics
Cardiotonic Agents – Therapeutic Use
Cardiotonic Agents/administration & dosage/metabolism/pharmacokinetics/therapeutic use
Coenzyme Q
Coenzyme Q – Administration and Dosage
Coenzyme Q – Metabolism
Coenzyme Q – Pharmacokinetics
Coenzyme Q – Therapeutic Use
Dadabayev Alisher R
Dietary Supplements
Electron Transport – Drug Effects
Electron Transport Complex II/chemistry/metabolism
Electron Transport Complex III/chemistry/metabolism
Electron Transport/drug effects
Heart – Drug Effects
Heart/drug effects
Heart/drug effects/enzymology/*metabolism
Hypoalphalipoproteinemias/physiopathology
Inborn Errors – Physiopathology
Injections
Intestinal Absorption
Intraperitoneal
Knockout
Latchoumycandane Calivarathan
Lesnefsky Edward J
Lipid Metabolism
Male
McIntyre Thomas M
Mice
Mitochondria
Mitochondria – Drug Effects
Mitochondria – Metabolism
Models
Myocardial Infarction – Etiology
Myocardial Infarction – Metabolism
Myocardial Infarction – Pathology
Myocardial Infarction – Therapy
Myocardial Infarction/etiology/metabolism/pathology/*therapy
Myocardial Reperfusion Injury – Blood
Myocardial Reperfusion Injury – Metabolism
Myocardial Reperfusion Injury – Pathology
Myocardial Reperfusion Injury – Prevention and Control
Myocardial Reperfusion Injury/blood/metabolism/pathology/prevention & control
Myocardium
Myocardium – Metabolism
Myocardium – Pathology
Myocardium/enzymology/*metabolism/pathology
Penn Marc S
Proteins
Proteins – Metabolism
The Journal of nutrition
Tissue Distribution
Ubiquinone/administration & dosage/*analogs & derivatives/metabolism/pharmacokinetics/therapeutic use
Yin Guotian
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1097/MOT.0b013e32835a5aad" target="_blank" rel="noreferrer noopener">http://doi.org/10.1097/MOT.0b013e32835a5aad</a>
Pages
663–669
Issue
6
Volume
17
Dublin Core
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Title
A name given to the resource
Are stem cells the teacher or the student?
Publisher
An entity responsible for making the resource available
Current opinion in organ transplantation
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-12
Subject
The topic of the resource
*Stem Cell Transplantation; *Stem Cells; Bone Marrow/physiopathology; Humans; Regeneration; Tissue Engineering; Wounds and Injuries/*physiopathology/*surgery
Creator
An entity primarily responsible for making the resource
Penn Marc S
Description
An account of the resource
PURPOSE OF REVIEW: Stem cell-based therapies for preventing and treating chronic end-organ dysfunction have captured the imagination of the lay public and spurred scientific and clinical development in multiple disciplines and disease states. The goal of this review is to build a framework around the different approaches being deployed to heal or treat end-organ dysfunction and discuss how within this framework future developments may occur. RECENT FINDINGS: In this review, we divide the development of regenerative therapies into two broad categories. The first 'Stem Cells as the Student' focuses on the fact that we need to coax/teach the stem cells to differentiate in an efficient manner into the cells of interest, then using tissue engineering, we need to integrate them in an appropriate delivery system/matrix, and then generate a blood supply, sufficient to allow for their survival following engraftment. In the second category 'Stem Cells as the Teacher,' we learn from studies on stem cell biology, critical pathways that are dysregulated in tissue repair. By identifying these critical pathways, we can develop drug and biologics that can enhance tissue repair and end-organ function. SUMMARY: Regenerative therapies have exciting potential to improve patient outcomes in a variety of acute and chronic disease states. There is significant excitement in general public, and the scientific and clinical communities. Early studies have been variably successful. As we move forward and understand the biology and engineering principles involved, significant advances with greater chances of success and efficacy will come.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/MOT.0b013e32835a5aad" target="_blank" rel="noreferrer noopener">10.1097/MOT.0b013e32835a5aad</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Stem Cell Transplantation
*Stem cells
2012
Bone Marrow/physiopathology
Current opinion in organ transplantation
Humans
Penn Marc S
Regeneration
Tissue Engineering
Wounds and Injuries/*physiopathology/*surgery
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1371/journal.pone.0068528" target="_blank" rel="noreferrer noopener">http://doi.org/10.1371/journal.pone.0068528</a>
Pages
e68528–e68528
Issue
7
Volume
8
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Bone marrow SSEA1+ cells support the myocardium in cardiac pressure overload.
Publisher
An entity responsible for making the resource available
PloS one
Date
A point or period of time associated with an event in the lifecycle of the resource
2013
1905-07
Subject
The topic of the resource
Male; Animals; Mice; Mesenchymal Stem Cells/cytology/metabolism; Ventricular Remodeling; *Bone Marrow Transplantation; Bone Marrow Cells/cytology/*metabolism; Cell Tracking; Lewis X Antigen/*metabolism; Myocardium/cytology/*metabolism/pathology; Myocytes; Cardiac/cytology/metabolism
Creator
An entity primarily responsible for making the resource
Finan Amanda; Sopko Nikolai; Dong Feng; Turturice Ben; Kiedrowski Matthew; Penn Marc S
Description
An account of the resource
RATIONALE: Stage specific embryonic antigen 1+ (SSEA1+) cells have been described as the most primitive mesenchymal progenitor cell in the bone marrow. Cardiac injury mobilizes SSEA1+ cells into the peripheral blood but their in vivo function has not been characterized. OBJECTIVE: We generated animals with chimeric bone marrow to determine the fate and function of bone marrow SSEA1+ cells in response to acute cardiac pressure overload. METHODS AND RESULTS: Lethally irradiated mice were transplanted with normal bone marrow where the wild-type SSEA1+ cells were replaced with green fluorescent protein (GFP) SSEA1+ cells. Cardiac injury was induced by trans-aortic constriction (TAC). We identified significant GFP+ cell engraftment into the myocardium after TAC. Bone marrow GFP+ SSEA1 derived cells acquired markers of endothelial lineage, but did not express markers of c-kit+ cardiac progenitor cells. The function of bone marrow SSEA1+ cells after TAC was determined by transplanting lethally irradiated mice with bone marrow depleted of SSEA1+ cells (SSEA1-BM). The cardiac function of SSEA1-BM mice declined at a greater rate after TAC compared to their complete bone marrow transplant counterparts and was associated with decreased bone marrow cell engraftment and greater vessel rarefication in the myocardium. CONCLUSIONS: These results provide evidence for the recruitment of endogenous bone marrow SSEA1+ cells to the myocardium after TAC. We demonstrate that, in vivo, bone marrow SSEA1+ cells have the differentiation potential to acquire endothelial lineage markers. We also show that bone marrow SSEA1+ deficiency is associated with a reduced compensatory capacity to cardiac pressure overload, suggesting their importance in cardiac homeostasis. These data demonstrate that bone marrow SSEA1+ cells are critical for sustaining vascular density and cardiac repair to pressure overload.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1371/journal.pone.0068528" target="_blank" rel="noreferrer noopener">10.1371/journal.pone.0068528</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Bone Marrow Transplantation
2013
Animals
Bone Marrow Cells/cytology/*metabolism
Cardiac/cytology/metabolism
Cell Tracking
Department of Integrative Medical Sciences
Dong Feng
Finan Amanda
Kiedrowski Matthew
Lewis X Antigen/*metabolism
Male
Mesenchymal Stem Cells/cytology/metabolism
Mice
Myocardium/cytology/*metabolism/pathology
Myocytes
NEOMED College of Medicine
Penn Marc S
PloS one
Sopko Nikolai
Turturice Ben
Ventricular Remodeling
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1016/j.yjmcc.2011.12.006" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.yjmcc.2011.12.006</a>
Pages
905–911
Issue
4
Volume
52
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Coronary collateral growth–back to the future.
Publisher
An entity responsible for making the resource available
Journal of molecular and cellular cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-04
Subject
The topic of the resource
Collateral Circulation/*physiology; Coronary Artery Disease/physiopathology/therapy; Coronary Circulation/physiology; Humans; Myocardial Ischemia/physiopathology/therapy; Neovascularization; Physiologic/physiology
Creator
An entity primarily responsible for making the resource
Chilian William M; Penn Marc S; Pung Yuh Fen; Dong Feng; Mayorga Maritza; Ohanyan Vahagn; Logan Suzanna; Yin Liya
Description
An account of the resource
The coronary collateral circulation is critically important as an adaptation of the heart to prevent the damage from ischemic insults. In their native state, collaterals in the heart would be classified as part of the microcirculation, existing as arterial-arterial anastomotic connections in the range of 30 to 100 muM in diameter. However, these vessels also show a propensity to remodel into components of the macrocirculation and can become arteries larger than 1000 muM in diameter. This process of outward remodeling is critically important in the adaptation of the heart to ischemia because the resistance to blood flow is inversely related to the fourth power of the diameter of the vessel. Thus, an expansion of a vessel from 100 to 1000 muM would reduce resistance (in this part of the circuit) to a negligible amount and enable delivery of flow to the region at risk. Our goal in this review is to highlight the voids in understanding this adaptation to ischemia-the growth of the coronary collateral circulation. In doing so we discuss the controversies and unknown aspects of the causal factors that stimulate growth of the collateral circulation, the role of genetics, and the role of endogenous stem and progenitor cells in the context of the normal, physiological situation and under more pathological conditions of ischemic heart disease or with some of the underlying risk factors, e.g., diabetes. The major conclusion of this review is that there are many gaps in our knowledge of coronary collateral growth and this knowledge is critical before the potential of stimulating collateralization in the hearts of patients can be realized. This article is part of a Special Issue entitled "Coronary Blood Flow".
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.yjmcc.2011.12.006" target="_blank" rel="noreferrer noopener">10.1016/j.yjmcc.2011.12.006</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2012
Chilian William M
Collateral Circulation/*physiology
Coronary Artery Disease/physiopathology/therapy
Coronary Circulation/physiology
Department of Integrative Medical Sciences
Dong Feng
Humans
Journal of molecular and cellular cardiology
Logan Suzanna
Mayorga Maritza
Myocardial Ischemia/physiopathology/therapy
NEOMED College of Medicine
Neovascularization
Ohanyan Vahagn
Penn Marc S
Physiologic/physiology
Pung Yuh Fen
Yin Liya
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajpheart.00449.2015" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.00449.2015</a>
Pages
H20–28
Issue
1
Volume
310
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Early upregulation of myocardial CXCR4 expression is critical for dimethyloxalylglycine-induced cardiac improvement in acute myocardial infarction.
Publisher
An entity responsible for making the resource available
American journal of physiology. Heart and circulatory physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-01
Subject
The topic of the resource
alpha Subunit/metabolism; Amino Acids; Animal; Animals; Apoptosis/drug effects; Cardiotonic Agents/*pharmacology; Cell Hypoxia; Cell Line; CXCR4/deficiency/genetics/*metabolism; Dicarboxylic/*pharmacology; Disease Models; Enzyme Inhibitors/pharmacology; hypoxia; Hypoxia-Inducible Factor 1; Hypoxia-Inducible Factor-Proline Dioxygenases/antagonists & inhibitors/metabolism; Inbred C57BL; Knockout; Left/*drug effects; Mice; myocardial infarction; Myocardial Infarction/*drug therapy/genetics/metabolism/pathology/physiopathology; Myocardium/*metabolism/pathology; Rats; Receptors; Recovery of Function; Signal Transduction/drug effects; stem cells; Stem Cells/drug effects/metabolism; Stroke Volume/drug effects; Time Factors; Up-Regulation; Ventricular Function
Creator
An entity primarily responsible for making the resource
Mayorga Mari; Kiedrowski Matthew; Shamhart Patricia; Forudi Farhad; Weber Kristal; Chilian William M; Penn Marc S; Dong Feng
Description
An account of the resource
The stromal cell-derived factor-1 (SDF-1):CXCR4 is important in myocardial repair. In this study we tested the hypothesis that early upregulation of cardiomyocyte CXCR4 (CM-CXCR4) at a time of high myocardial SDF-1 expression could be a strategy to engage the SDF-1:CXCR4 axis and improve cardiac repair. The effects of the hypoxia inducible factor (HIF) hydroxylase inhibitor dimethyloxalylglycine (DMOG) on CXCR4 expression was tested on H9c2 cells. In mice a myocardial infarction (MI) was produced in CM-CXCR4 null and wild-type controls. Mice were randomized to receive injection of DMOG (DMOG group) or saline (Saline group) into the border zone after MI. Protein and mRNA expression of CM-CXCR4 were quantified. Echocardiography was used to assess cardiac function. During hypoxia, DMOG treatment increased CXCR4 expression of H9c2 cells by 29 and 42% at 15 and 24 h, respectively. In vivo DMOG treatment increased
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.00449.2015" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.00449.2015</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2016
alpha Subunit/metabolism
American journal of physiology. Heart and circulatory physiology
Amino Acids
Animal
Animals
Apoptosis/drug effects
Cardiotonic Agents/*pharmacology
Cell Hypoxia
Cell Line
Chilian William M
CXCR4/deficiency/genetics/*metabolism
Department of Integrative Medical Sciences
Dicarboxylic/*pharmacology
Disease Models
Dong Feng
Enzyme Inhibitors/pharmacology
Forudi Farhad
hypoxia
Hypoxia-Inducible Factor 1
Hypoxia-Inducible Factor-Proline Dioxygenases/antagonists & inhibitors/metabolism
Inbred C57BL
Kiedrowski Matthew
Knockout
Left/*drug effects
Mayorga Mari
Mice
myocardial infarction
Myocardial Infarction/*drug therapy/genetics/metabolism/pathology/physiopathology
Myocardium/*metabolism/pathology
NEOMED College of Medicine
Penn Marc S
Rats
Receptors
Recovery of Function
Shamhart Patricia
Signal Transduction/drug effects
stem cells
Stem Cells/drug effects/metabolism
Stroke Volume/drug effects
Time Factors
Up-Regulation
Ventricular Function
Weber Kristal
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1097/SPV.0000000000000394" target="_blank" rel="noreferrer noopener">http://doi.org/10.1097/SPV.0000000000000394</a>
Pages
449–456
Issue
6
Volume
23
Dublin Core
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Title
A name given to the resource
Effect of Pregnancy and Delivery on Cytokine Expression in a Mouse Model of Pelvic Organ Prolapse.
Publisher
An entity responsible for making the resource available
Female pelvic medicine & reconstructive surgery
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-12
Subject
The topic of the resource
Amino Acid Oxidoreductases/*genetics/metabolism; Animal; Animals; Chemokine CCL7/genetics/metabolism; Chemokine CXCL12/genetics/metabolism; Delivery; Female; Humans; Knockout; Mice; Models; Obstetric/*adverse effects/methods; Pelvic Organ Prolapse/*genetics/metabolism/pathology; Pregnancy; Reverse Transcriptase Polymerase Chain Reaction; Urethra/metabolism; Urinary Bladder/metabolism; Vagina/metabolism
Creator
An entity primarily responsible for making the resource
Couri Bruna M; Lenis Andrew T; Borazjani Ali; Balog Brian M; Kuang Mei; Butler Robert S; Penn Marc S; Damaser Margot S
Description
An account of the resource
OBJECTIVES: The aim of this study was to determine the effect of pregnancy and delivery mode on cytokine expression in the pelvic organs and serum of lysyl oxidase like-1 knockout (LOXL1 KO) mice, which develop pelvic organ prolapse after delivery. METHODS: Bladder, urethra, vagina, rectum, and blood were harvested from female LOXL1 KO mice during pregnancy, after vaginal or cesarean delivery, and from sham cesarean and unmanipulated controls. Pelvic organs and blood were also harvested from pregnant and vaginally delivered wild-type (WT) mice and from unmanipulated female virgin WT controls. Specimens were assessed using quantitative real-time reverse transcription polymerase chain reaction and/or enzyme-linked immunosorbent assay. RESULTS: Both CXCL12 and CCL7 mRNA were significantly up-regulated in the vagina, urethra, bladder, and rectum of pregnant LOXL1 KO mice compared with pregnant WT mice, suggesting systemic dysregulation of both of these cytokines in LOXL1 KO mice as a response to pregnancy.The differences in cytokine expression between LOXL1 KO and WT mice in pregnancy persisted after vaginal delivery. CCL7 gene expression increases faster and to a greater extent in LOXL1 KO mice, translating to longer lasting increases in CCL7 in serum of LOXL1 KO mice after vaginal delivery, compared with pregnant mice. CONCLUSIONS: Lysyl oxidase like-1 KO mice have an increased cytokine response to pregnancy perhaps because they are less able to reform and re-cross-link stretched elastin to accommodate pups, and this resultant tissue stretches during pregnancy. The up-regulation of CCL7 after delivery could provide an indicator of level of childbirth injury, to which the urethra and vagina seem to be particularly vulnerable.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/SPV.0000000000000394" target="_blank" rel="noreferrer noopener">10.1097/SPV.0000000000000394</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
Amino Acid Oxidoreductases/*genetics/metabolism
Animal
Animals
Balog Brian M
Borazjani Ali
Butler Robert S
Chemokine CCL7/genetics/metabolism
Chemokine CXCL12/genetics/metabolism
Couri Bruna M
Damaser Margot S
Delivery
Female
Female pelvic medicine & reconstructive surgery
Humans
Knockout
Kuang Mei
Lenis Andrew T
Mice
Models
Obstetric/*adverse effects/methods
Pelvic Organ Prolapse/*genetics/metabolism/pathology
Penn Marc S
Pregnancy
Reverse Transcriptase Polymerase Chain Reaction
Urethra/metabolism
Urinary Bladder/metabolism
Vagina/metabolism
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1152/ajprenal.00510.2014" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajprenal.00510.2014</a>
Pages
F92–F100
Issue
2
Volume
308
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Mesenchymal stem cells and their secretome partially restore nerve and urethral function in a dual muscle and nerve injury stress urinary incontinence model.
Publisher
An entity responsible for making the resource available
American journal of physiology. Renal physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-01
Subject
The topic of the resource
*Mesenchymal Stem Cell Transplantation; Animals; Conditioned; Culture Media; elastin; external urethral sphincter; Female; Injections; Intraperitoneal; Intravenous; Mesenchymal Stem Cells/metabolism; paracrine action; Parturition; pudendal nerve; Pudendal Nerve/injuries/*physiology; Rats; Sprague-Dawley; Stress/etiology/*prevention & control; Urethra/injuries/*physiology; urinary incontinence; Urinary Incontinence
Creator
An entity primarily responsible for making the resource
Deng Kangli; Lin Dan Li; Hanzlicek Brett; Balog Brian; Penn Marc S; Kiedrowski Matthew J; Hu Zhiquan; Ye Zhangqun; Zhu Hui; Damaser Margot S
Description
An account of the resource
Childbirth injures muscles and nerves responsible for urinary continence. Mesenchymal stem cells (MSCs) or their secretome given systemically could provide therapeutic benefit for this complex multisite injury. We investigated whether MSCs or their secretome, as collected from cell culture, facilitate recovery from simulated childbirth injury. Age-matched female Sprague-Dawley rats received pudendal nerve crush and vaginal distension (PNC+VD) and a single intravenous (iv) injection of 2 million MSCs or saline. Controls received sham injury and iv saline. Additional rats received PNC+VD and a single intraperitoneal (ip) injection of concentrated media conditioned by MSCs (CCM) or concentrated control media (CM). Controls received a sham injury and ip CM. Urethral and nerve function were assessed with leak point pressure (LPP) and pudendal nerve sensory branch potential (PNSBP) recordings 3 wk after injury. Urethral and pudendal nerve anatomy were assessed qualitatively by blinded investigators. Quantitative data were analyzed using one-way ANOVA and Holm-Sidak post hoc tests with P \textless 0.05 indicating significant differences. Both LPP and PNSBP were significantly decreased 3 wk after PNC+VD with saline or CM compared with sham-injured rats, but not with MSC or CCM. Elastic fiber density in the urethra increased and changed in orientation after PNC+VD, with a greater increase in elastic fibers with MSC or CCM. Pudendal nerve fascicles were less dense and irregularly shaped after PNC+VD and had reduced pathology with MSC or CCM. MSC and CCM provide similar protective effects after PNC+VD, suggesting that MSCs act via their secretions in this dual muscle and nerve injury.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajprenal.00510.2014" target="_blank" rel="noreferrer noopener">10.1152/ajprenal.00510.2014</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Mesenchymal Stem Cell Transplantation
2015
American journal of physiology. Renal physiology
Animals
Balog Brian
Conditioned
Culture Media
Damaser Margot S
Deng Kangli
elastin
external urethral sphincter
Female
Hanzlicek Brett
Hu Zhiquan
Injections
Intraperitoneal
Intravenous
Kiedrowski Matthew J
Lin Dan Li
Mesenchymal Stem Cells/metabolism
paracrine action
Parturition
Penn Marc S
pudendal nerve
Pudendal Nerve/injuries/*physiology
Rats
Sprague-Dawley
Stress/etiology/*prevention & control
Urethra/injuries/*physiology
Urinary Incontinence
Ye Zhangqun
Zhu Hui
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/CIRCULATIONAHA.111.082453" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCULATIONAHA.111.082453</a>
Pages
314–324
Issue
3
Volume
126
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Myocardial CXCR4 expression is required for mesenchymal stem cell mediated repair following acute myocardial infarction.
Publisher
An entity responsible for making the resource available
Circulation
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-07
Subject
The topic of the resource
Animals; Apoptosis/physiology; Cardiac/cytology/physiology; Cell Movement/physiology; Chemokine CXCL12/*metabolism; Coronary Circulation/physiology; CXCR4/*genetics/metabolism; Gene Expression/physiology; Green Fluorescent Proteins/genetics; Inbred C57BL; Knockout; Mesenchymal Stem Cell Transplantation/*methods; Mesenchymal Stem Cells/*metabolism; Mice; Myocardial Infarction/genetics/pathology/*therapy; Myocardium/cytology; Myocytes; Paracrine Communication/physiology; Receptors; Ventricular Remodeling/physiology
Creator
An entity primarily responsible for making the resource
Dong Feng; Harvey James; Finan Amanda; Weber Kristal; Agarwal Udit; Penn Marc S
Description
An account of the resource
BACKGROUND: Overexpression of stromal cell-derived factor-1 in injured tissue leads to improved end-organ function. In this study, we quantify the local trophic effects of mesenchymal stem cell (MSC) stromal cell-derived factor-1 release on the effects of MSC engraftment in the myocardium after acute myocardial infarction. METHODS AND RESULTS: Conditional cardiac myocyte CXCR4 (CM-CXCR4) null mice were generated by use of tamoxifen-inducible cardiac-specific cre by crossing CXCR4 floxed with MCM-cre mouse. Studies were performed in littermates with (CM-CXCR4 null) or without (control) tamoxifen injection 3 weeks before acute myocardial infarction. One day after acute myocardial infarction, mice received 100,000 MSC or saline via tail vein. We show alpha-myosin heavy chain MerCreMer and the MLC-2v promoters are active in cardiac progenitor cells. MSC engraftment in wild-type mice decreased terminal deoxynucleotidyltransferase-mediated dUTP nick-end labeling positive CM (-44%, P\textless0.01), increased cardiac progenitor cell recruitment (100.9%, P\textless0.01), and increased cardiac myosin-positive area (39%, P\textless0.05) at 4, 7, and 21 days after acute myocardial infarction, respectively. MSC in wild-type mice resulted in 107.4% (P\textless0.05) increase in ejection fraction in comparison with 25.9% (P=NS) increase in CM-CXCR4 null mice. These differences occurred despite equivalent increases (16%) in vascular density in response to MSC infusion in wild-type and
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCULATIONAHA.111.082453" target="_blank" rel="noreferrer noopener">10.1161/CIRCULATIONAHA.111.082453</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2012
Agarwal Udit
Animals
Apoptosis/physiology
Cardiac/cytology/physiology
Cell Movement/physiology
Chemokine CXCL12/*metabolism
Circulation
Coronary Circulation/physiology
CXCR4/*genetics/metabolism
Department of Integrative Medical Sciences
Dong Feng
Finan Amanda
Gene Expression/physiology
Green Fluorescent Proteins/genetics
Harvey James
Inbred C57BL
Knockout
Mesenchymal Stem Cell Transplantation/*methods
Mesenchymal Stem Cells/*metabolism
Mice
Myocardial Infarction/genetics/pathology/*therapy
Myocardium/cytology
Myocytes
NEOMED College of Medicine
Paracrine Communication/physiology
Penn Marc S
Receptors
Ventricular Remodeling/physiology
Weber Kristal
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/CIRCRESAHA.116.310105" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.116.310105</a>
Pages
1256–1257
Issue
12
Volume
119
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Role of Inflammation in Modulating Thrombotic-Fibrinolytic Balance in Venous Thrombosis.
Publisher
An entity responsible for making the resource available
Circulation research
Date
A point or period of time associated with an event in the lifecycle of the resource
2016
2016-12
Subject
The topic of the resource
*chemokines; *Editorials; *fibrinolytic therapy; *inflammation; *T-lymphocytes; *Thrombosis; *venous thrombosis; *Venous Thrombosis; Fibrinolytic Agents; Humans; Inflammation; Thrombolytic Therapy
Creator
An entity primarily responsible for making the resource
Penn Marc S; Igwe Chinedu
Identifier
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<a href="http://doi.org/10.1161/CIRCRESAHA.116.310105" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.116.310105</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*chemokines
*Editorials
*fibrinolytic therapy
*Inflammation
*T-lymphocytes
*Thrombosis
*venous thrombosis
2016
Circulation research
Fibrinolytic Agents
Humans
Igwe Chinedu
Inflammation
Penn Marc S
Thrombolytic Therapy
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1002/sctm.17-0172" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/sctm.17-0172</a>
Pages
115–124
Issue
1
Volume
7
Dublin Core
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Title
A name given to the resource
Role of SDF-1:CXCR4 in Impaired Post-Myocardial Infarction Cardiac Repair in Diabetes.
Publisher
An entity responsible for making the resource available
Stem cells translational medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-01
Subject
The topic of the resource
Cardiac; Cell therapy; Diabetes; Stem cells; Stromal derived factor-1
Creator
An entity primarily responsible for making the resource
Mayorga Maritza E; Kiedrowski Matthew; McCallinhart Patricia; Forudi Farhad; Ockunzzi Jeremiah; Weber Kristal; Chilian William; Penn Marc S; Dong Feng
Description
An account of the resource
Diabetes is a risk factor for worse outcomes following acute myocardial infarction (AMI). In this study, we tested the hypothesis that SDF-1:CXCR4 expression is compromised in post-AMI in diabetes, and that reversal of this defect can reverse the adverse effects of diabetes. Mesenchymal stem cells (MSC) isolated from green fluorescent protein (GFP) transgenic mice (control MSC) were induced to overexpress stromal cell-derived factor-1 (SDF-1). SDF-1 expression in control MSC and SDF-1-overexpressing MSC (SDF-1:MSC) were quantified using enzyme-linked immunosorbent assay (ELISA). AMI was induced on db/db and control mice. Mice were randomly selected to receive infusion of control MSC, SDF-1:MSC, or saline into the border zone after AMI. Serial echocardiography was used to assess cardiac function. SDF-1 and CXCR4 mRNA expression in the infarct zone of db/db mice and control mice were quantified. Compared to control mice, SDF-1 levels were decreased 82%, 91%, and 45% at baseline, 1 day and 3 days post-AMI in db/db mice, respectively. CXCR4 levels are increased 233% at baseline and 54% 5 days post-AMI in db/db mice. Administration of control MSC led to a significant improvement in ejection fraction (EF) in control mice but not in db/db mice 21 days after AMI. In contrast, administration of SDF-1:MSC produced a significant improvement in EF in both control mice and db/db mice 21 days after AMI. The
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1002/sctm.17-0172" target="_blank" rel="noreferrer noopener">10.1002/sctm.17-0172</a>
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2018
Cardiac
Cell therapy
Chilian William
Department of Integrative Medical Sciences
Diabetes
Dong Feng
Forudi Farhad
Kiedrowski Matthew
Mayorga Maritza E
McCallinhart Patricia
NEOMED College of Medicine
Ockunzzi Jeremiah
Penn Marc S
stem cells
Stem cells translational medicine
Stromal derived factor-1
Weber Kristal
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/CIRCRESAHA.116.309904" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.116.309904</a>
Pages
1075–1077
Issue
7
Volume
120
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
The Unraveling of the Matryoshka Doll.
Publisher
An entity responsible for making the resource available
Circulation research
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-03
Subject
The topic of the resource
chemokines; exosomes; heart failure; myocardial infarction; stem cells
Creator
An entity primarily responsible for making the resource
Penn Marc S
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.116.309904" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.116.309904</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2017
chemokines
Circulation research
Exosomes
Heart failure
myocardial infarction
Penn Marc S
stem cells
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
URL Address
<a href="http://doi.org/10.1161/CIRCRESAHA.116.309904" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.116.309904</a>
Rights
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
Pages
1075-1077
Issue
7
Volume
120
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
The Unraveling of the Matryoshka Doll.
Publisher
An entity responsible for making the resource available
Circulation research
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-03
Subject
The topic of the resource
Adult; Humans; Gene Expression; *stem cells; *chemokines; Stem Cell Transplantation/*methods; *exosomes; *heart failure; *myocardial infarction; Adult Stem Cells/metabolism/*transplantation; Exosomes/genetics/metabolism; Heart Diseases/physiopathology/*therapy; MicroRNAs/genetics/metabolism; Regenerative Medicine/methods/trends
Creator
An entity primarily responsible for making the resource
Penn Marc S
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.116.309904" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.116.309904</a>
*chemokines
*exosomes
*heart failure
*Myocardial infarction
*Stem cells
2017
Adult
Adult Stem Cells/metabolism/*transplantation
Circulation research
Exosomes/genetics/metabolism
Gene Expression
Heart Diseases/physiopathology/*therapy
Humans
MicroRNAs/genetics/metabolism
Penn Marc S
Regenerative Medicine/methods/trends
Stem Cell Transplantation/*methods