1
40
7
-
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.neuropharm.2017.07.020" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.neuropharm.2017.07.020</a>
Pages
189–196
Volume
125
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
Valproate increases dopamine transporter expression through histone acetylation and enhanced promoter binding of Nurr1.
Publisher
An entity responsible for making the resource available
Neuropharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
2017-10
Subject
The topic of the resource
Acetylation/drug effects; Animals; Butyrates/pharmacology; Cell Line; Cell Survival/drug effects; Dopamine Plasma Membrane Transport Proteins/*metabolism; Dopamine transporter; Dopaminergic Neurons/cytology/drug effects/metabolism; Dose-Response Relationship; Drug; Epigenesis; Epigenetics; Genetic; Genetic/drug effects; Group A; HDAC; Histone deacetylase; Histone Deacetylase Inhibitors/*pharmacology; Histone Deacetylases/metabolism; Histones/*drug effects/metabolism; Homeodomain Proteins/metabolism; Hydroxamic Acids/pharmacology; Member 2/*metabolism; Messenger/metabolism; Nuclear Receptor Subfamily 4; Nurr1; Pitx3; Promoter Regions; Rats; RNA; Transcription Factors/metabolism; Valproate; Valproic Acid/*pharmacology
Creator
An entity primarily responsible for making the resource
Green Ashley L; Zhan Le; Eid Aseel; Zarbl Helmut; Guo Grace L; Richardson Jason R
Description
An account of the resource
The dopamine transporter (DAT) is the key regulator of dopaminergic transmission and is a target of several xenobiotics, including pesticides and pharmacological agents. Previously, we identified a prominent role for histone deacetylases in the regulation of DAT expression. Here, we utilized a rat dopaminergic cell line (N27) to probe the responsiveness of DAT mRNA expression to inhibitors of histone acetylation. Inhibition of histone deacetylases (HDACs) by valproate, butyrate and Trichostatin A led to a 3-10-fold increase in DAT mRNA expression, a 50% increase in protein levels, which were accompanied by increased H3 acetylation levels. To confirm the mechanism of valproate-mediated increase in DAT mRNA, chromatin immunoprecipitation (ChIP) assays were used and demonstrated a significant increase in enrichment of acetylation of histone 3 on lysines 9 and 14 (H3K9/K14ac) in the DAT promoter. Expression of Nurr1 and Pitx3, key regulators of DAT expression, were increased following valproate treatment and Nurr1 binding was enriched in the DAT promoter. Together, these results indicate that histone acetylation and subsequent enhancement of transcription factor binding are plausible mechanisms for DAT regulation by valproate and, perhaps, by other xenobiotics.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.neuropharm.2017.07.020" target="_blank" rel="noreferrer noopener">10.1016/j.neuropharm.2017.07.020</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).
2017
Acetylation/drug effects
Animals
Butyrates/pharmacology
Cell Line
Cell Survival/drug effects
Department of Pharmaceutical Sciences
Dopamine Plasma Membrane Transport Proteins/*metabolism
Dopamine transporter
Dopaminergic Neurons/cytology/drug effects/metabolism
Dose-Response Relationship
Drug
Eid Aseel
Epigenesis
Epigenetics
Genetic
Genetic/drug effects
Green Ashley L
Group A
Guo Grace L
HDAC
Histone deacetylase
Histone Deacetylase Inhibitors/*pharmacology
Histone Deacetylases/metabolism
Histones/*drug effects/metabolism
Homeodomain Proteins/metabolism
Hydroxamic Acids/pharmacology
Member 2/*metabolism
Messenger/metabolism
NEOMED College of Pharmacy
Neuropharmacology
Nuclear Receptor Subfamily 4
Nurr1
Pitx3
Promoter Regions
Rats
Richardson Jason R
RNA
Transcription Factors/metabolism
Valproate
Valproic Acid/*pharmacology
Zarbl Helmut
Zhan Le
-
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.phrs.2017.08.007" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.phrs.2017.08.007</a>
Pages
73–79
Volume
128
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
Epigenetics in osteoarthritis: Potential of HDAC inhibitors as therapeutics.
Publisher
An entity responsible for making the resource available
Pharmacological research
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-02
Subject
The topic of the resource
*DNA methylation; *Epigenetics; *HDACs; *lncRNA; *miRNA; *Osteoarthritis; Animals; Epigenesis; Genetic; Histone Deacetylase Inhibitors/*therapeutic use; Humans; Osteoarthritis/*drug therapy/*genetics
Creator
An entity primarily responsible for making the resource
Khan Nazir M; Haqqi Tariq M
Description
An account of the resource
Osteoarthritis (OA) is the most common joint disease and the leading cause of chronic disability in middle-aged and older populations worldwide. The development of disease modifying therapy for OA is in its infancy largely because the regulatory mechanisms for the molecular effectors of OA pathogenesis are poorly understood. Recent studies identified epigenetic events as a critical regulator of molecular players involved in the induction and development of OA. Epigenetic mechanisms include DNA methylation, non-coding RNA and histone modifications. The aim of this review is to briefly highlight the recent advances in the epigenetics of cartilage and potential of HDACs (Histone deacetylases) inhibitors in the therapeutic management of OA. We summarize the recent studies utilizing HDAC inhibitors as potential therapeutics for inhibiting disease progression and preventing the cartilage destruction in OA. HDACs control normal cartilage development and homeostasis and understanding the impact of HDACs inhibitors on the disease pathogenesis is of interest because of its importance in affecting overall cartilage health and homeostasis. These findings also shed new light on cartilage disease pathophysiology and provide substantial evidence that HDACs may be potential novel therapeutic targets in OA.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.phrs.2017.08.007" target="_blank" rel="noreferrer noopener">10.1016/j.phrs.2017.08.007</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).
*DNA methylation
*Epigenetics
*HDACs
*lncRNA
*miRNA
*OSTEOARTHRITIS
2018
Animals
Department of Anatomy & Neurobiology
Epigenesis
Genetic
Haqqi Tariq M
Histone Deacetylase Inhibitors/*therapeutic use
Humans
Khan Nazir M
NEOMED College of Medicine
Osteoarthritis/*drug therapy/*genetics
Pharmacological research
-
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/10.1194/jlr.M002782" target="_blank" rel="noreferrer noopener">http://doi.org/10.1194/jlr.M002782</a>
Pages
832–842
Issue
4
Volume
51
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
Glucose stimulates cholesterol 7alpha-hydroxylase gene transcription in human hepatocytes.
Publisher
An entity responsible for making the resource available
Journal of lipid research
Date
A point or period of time associated with an event in the lifecycle of the resource
2010
2010-04
Subject
The topic of the resource
*Gene Expression Regulation; Acetylation; AMP-Activated Protein Kinases/metabolism; ATP Citrate (pro-S)-Lyase/genetics/metabolism; Bile Acids and Salts/metabolism; Cells; Cholesterol 7-alpha-Hydroxylase/genetics/*metabolism; Cultured; DNA-Binding Proteins/metabolism; Enzymologic; Epigenesis; Genes; Genetic; Glucose/*administration & dosage; Hep G2 Cells; Hepatocyte Nuclear Factor 4/metabolism; Hepatocytes/*enzymology/metabolism; Histones/metabolism; Humans; Hyperglycemia/enzymology/*metabolism; Messenger/metabolism; Methylation; Reporter; RNA; RNA Interference
Creator
An entity primarily responsible for making the resource
Li Tiangang; Chanda Dipanjan; Zhang Yanqiao; Choi Hueng-Sik; Chiang John Y L
Description
An account of the resource
Bile acids play important roles in the regulation of lipid, glucose, and energy homeostasis. Recent studies suggest that glucose regulates gene transcription in the liver. The aim of this study was to investigate the potential role of glucose in regulation of bile acid synthesis in human hepatocytes. High glucose stimulated bile acid synthesis and induced mRNA expression of cholesterol 7alpha-hydroxylase (CYP7A1), the key regulatory gene in bile acid synthesis. Activation of an AMP-activated protein kinase (AMPK) decreased CYP7A1 mRNA, hepatocyte nuclear factor 4alpha (HNF4alpha) protein, and binding to CYP7A1 chromatin. Glucose increased ATP levels to inhibit AMPK and induce HNF4alpha to stimulate CYP7A1 gene transcription. Furthermore, glucose increased histone acetylation and decreased H3K9 di- and tri-methylation in the CYP7A1 chromatin. Knockdown of ATP-citrate lyase, which converts citrate to acetyl-CoA, decreased histone acetylation and attenuated glucose induction of CYP7A1 mRNA expression. These results suggest that glucose signaling also induces CYP7A1 gene transcription by epigenetic regulation of the histone acetylation status. This study uncovers a novel link between hepatic glucose metabolism and bile acid synthesis. Glucose induction of bile acid synthesis may have an important implication in metabolic control of glucose, lipid, and energy homeostasis under normal and diabetic conditions.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1194/jlr.M002782" target="_blank" rel="noreferrer noopener">10.1194/jlr.M002782</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).
*Gene Expression Regulation
2010
Acetylation
AMP-Activated Protein Kinases/metabolism
ATP Citrate (pro-S)-Lyase/genetics/metabolism
Bile Acids and Salts/metabolism
Cells
Chanda Dipanjan
Chiang John Y L
Choi Hueng-Sik
Cholesterol 7-alpha-Hydroxylase/genetics/*metabolism
Cultured
Department of Integrative Medical Sciences
DNA-Binding Proteins/metabolism
Enzymologic
Epigenesis
Genes
Genetic
Glucose/*administration & dosage
Hep G2 Cells
Hepatocyte Nuclear Factor 4/metabolism
Hepatocytes/*enzymology/metabolism
Histones/metabolism
Humans
Hyperglycemia/enzymology/*metabolism
Journal of lipid research
Li Tiangang
Messenger/metabolism
Methylation
NEOMED College of Medicine
Reporter
RNA
RNA Interference
Zhang Yanqiao
-
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/10.1074/jbc.M111.305789" target="_blank" rel="noreferrer noopener">http://doi.org/10.1074/jbc.M111.305789</a>
Pages
1861–1873
Issue
3
Volume
287
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
Glucose and insulin induction of bile acid synthesis: mechanisms and implication in diabetes and obesity.
Publisher
An entity responsible for making the resource available
The Journal of biological chemistry
Date
A point or period of time associated with an event in the lifecycle of the resource
2012
2012-01
Subject
The topic of the resource
*Gene Expression Regulation; Animals; Bile Acids and Salts/*biosynthesis; Cholesterol 7-alpha-Hydroxylase/genetics/*metabolism; Cytoplasmic and Nuclear/genetics/metabolism; Diabetes Mellitus; Dietary Fats/administration & dosage/adverse effects; Enzymologic; Epigenesis; Experimental/genetics/*metabolism; Fasting/metabolism; Genetic/genetics; Glucose/*metabolism/pharmacology; Insulin/*metabolism; Mice; Obesity/etiology/genetics/*metabolism; Postprandial Period/genetics; Receptors; Sweetening Agents/pharmacology; Transgenic
Creator
An entity primarily responsible for making the resource
Li Tiangang; Francl Jessica M; Boehme Shannon; Ochoa Adrian; Zhang Youcai; Klaassen Curtis D; Erickson Sandra K; Chiang John Y L
Description
An account of the resource
Bile acids facilitate postprandial absorption of nutrients. Bile acids also activate the farnesoid X receptor (FXR) and the G protein-coupled receptor TGR5 and play a major role in regulating lipid, glucose, and energy metabolism. Transgenic expression of cholesterol 7alpha-hydroxylase (CYP7A1) prevented high fat diet-induced diabetes and obesity in mice. In this study, we investigated the nutrient effects on bile acid synthesis. Refeeding of a chow diet to fasted mice increased CYP7A1 expression, bile acid pool size, and serum bile acids in wild type and humanized CYP7A1-transgenic mice. Chromatin immunoprecipitation assays showed that glucose increased histone acetylation and decreased histone methylation on the CYP7A1 gene promoter. Refeeding also induced CYP7A1 in fxr-deficient mice, indicating that FXR signaling did not play a role in postprandial regulation of bile acid synthesis. In streptozocin-induced type I diabetic mice and genetically obese type II diabetic ob/ob mice, hyperglycemia increased histone acetylation status on the CYP7A1 gene promoter, leading to elevated basal Cyp7a1 expression and an enlarged bile acid pool with altered bile acid composition. However, refeeding did not further increase CYP7A1 expression in diabetic mice. In summary, this study demonstrates that glucose and insulin are major postprandial factors that induce CYP7A1 gene expression and bile acid synthesis. Glucose induces CYP7A1 gene expression mainly by epigenetic mechanisms. In diabetic mice, CYP7A1 chromatin is hyperacetylated, and fasting to refeeding response is impaired and may exacerbate metabolic disorders in diabetes.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1074/jbc.M111.305789" target="_blank" rel="noreferrer noopener">10.1074/jbc.M111.305789</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).
*Gene Expression Regulation
2012
Animals
Bile Acids and Salts/*biosynthesis
Boehme Shannon
Chiang John Y L
Cholesterol 7-alpha-Hydroxylase/genetics/*metabolism
Cytoplasmic and Nuclear/genetics/metabolism
Department of Integrative Medical Sciences
Diabetes Mellitus
Dietary Fats/administration & dosage/adverse effects
Enzymologic
Epigenesis
Erickson Sandra K
Experimental/genetics/*metabolism
Fasting/metabolism
Francl Jessica M
Genetic/genetics
Glucose/*metabolism/pharmacology
Insulin/*metabolism
Klaassen Curtis D
Li Tiangang
Mice
NEOMED College of Medicine
Obesity/etiology/genetics/*metabolism
Ochoa Adrian
Postprandial Period/genetics
Receptors
Sweetening Agents/pharmacology
The Journal of biological chemistry
Transgenic
Zhang Youcai
-
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.jacc.2015.07.037" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.jacc.2015.07.037</a>
Pages
1378–1391
Issue
12
Volume
66
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
Cardiovascular Effects of Exposure to Cigarette Smoke and Electronic Cigarettes: Clinical Perspectives From the Prevention of Cardiovascular Disease Section Leadership Council and Early Career Councils of the American College of Cardiology.
Publisher
An entity responsible for making the resource available
Journal of the American College of Cardiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2015
2015-09
Subject
The topic of the resource
atherogenesis; Cardiovascular Diseases – Etiology; Cardiovascular Diseases/*etiology; Electronic Cigarettes – Adverse Effects; Electronic Nicotine Delivery Systems/*adverse effects; Epigenesis; Genes; Genetic; genetic and epigenetic effects; Humans; Impact of Events Scale; Scales; smoke-free legislation; Smoking – Complications; Smoking – Legislation and Jurisprudence – United States; Smoking Cessation; Smoking/*adverse effects/legislation & jurisprudence; thrombosis; tobacco cessation; United States
Creator
An entity primarily responsible for making the resource
Morris Pamela B; Ference Brian A; Jahangir Eiman; Feldman Dmitriy N; Ryan John J; Bahrami Hossein; El-Chami Mikhael F; Bhakta Shyam; Winchester David E; Al-Mallah Mouaz H; Sanchez Shields Monica; Deedwania Prakash; Mehta Laxmi S; Phan Binh An P; Benowitz Neal L
Description
An account of the resource
Cardiovascular morbidity and mortality as a result of inhaled tobacco products continues to be a global healthcare crisis, particularly in low- and middle-income nations lacking the infrastructure to develop and implement effective public health policies limiting tobacco use. Following initiation of public awareness campaigns 50 years ago in the United States, considerable success has been achieved in reducing the prevalence of cigarette smoking and exposure to secondhand smoke. However, there has been a slowing of cessation rates in the United States during recent years, possibly caused by high residual addiction or fatigue from cessation messaging. Furthermore, tobacco products have continued to evolve faster than the scientific understanding of their biological effects. This review considers selected updates on the genetics and epigenetics of smoking behavior and associated cardiovascular risk, mechanisms of atherogenesis and thrombosis, clinical effects of smoking and benefits of cessation, and potential impact of electronic cigarettes on cardiovascular health.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.jacc.2015.07.037" target="_blank" rel="noreferrer noopener">10.1016/j.jacc.2015.07.037</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).
2015
Al-Mallah Mouaz H
atherogenesis
Bahrami Hossein
Benowitz Neal L
Bhakta Shyam
Cardiovascular Diseases – Etiology
Cardiovascular Diseases/*etiology
Deedwania Prakash
Department of Internal Medicine
El-Chami Mikhael F
Electronic Cigarettes – Adverse Effects
Electronic Nicotine Delivery Systems/*adverse effects
Epigenesis
Feldman Dmitriy N
Ference Brian A
Genes
Genetic
genetic and epigenetic effects
Humans
Impact of Events Scale
Jahangir Eiman
Journal of the American College of Cardiology
Mehta Laxmi S
Morris Pamela B
NEOMED College of Medicine
Phan Binh An P
Ryan John J
Sanchez Shields Monica
Scales
smoke-free legislation
Smoking – Complications
Smoking – Legislation and Jurisprudence – United States
Smoking Cessation
Smoking/*adverse effects/legislation & jurisprudence
Thrombosis
tobacco cessation
United States
Winchester David E
-
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/10.1186/s13148-017-0416-5" target="_blank" rel="noreferrer noopener">http://doi.org/10.1186/s13148-017-0416-5</a>
Pages
117–117
Volume
9
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
Turnover of histones and histone variants in postnatal rat brain: effects of alcohol exposure.
Publisher
An entity responsible for making the resource available
Clinical epigenetics
Date
A point or period of time associated with an event in the lifecycle of the resource
2017
1905-07
Subject
The topic of the resource
*2H2O-labeling; *Brain; *Genetic Variation; *Histone; *Mass spectrometry; *Post-translational modifications; *Postnatal alcohol exposure; *Turnover; Acetylation; Animal; Animals; Cell Proliferation; Disease Models; DNA Damage; Epigenesis; Female; Fetal Alcohol Spectrum Disorders/genetics/*metabolism; Genetic; Histones/*genetics/*metabolism; Humans; Post-Translational; Pregnancy; Protein Processing; Proteomics/*methods; Rats; Sprague-Dawley
Creator
An entity primarily responsible for making the resource
Rachdaoui Nadia; Li Ling; Willard Belinda; Kasumov Takhar; Previs Stephen; Sarkar Dipak
Description
An account of the resource
BACKGROUND: Alcohol consumption during pregnancy is a significant public health problem and can result in a continuum of adverse outcomes to the fetus known as fetal alcohol spectrum disorders (FASD). Subjects with FASD show significant neurological deficits, ranging from microencephaly, neurobehavioral, and mental health problems to poor social adjustment and stress tolerance. Neurons are particularly sensitive to alcohol exposure. The neurotoxic action of alcohol, i.e., through ROS production, induces DNA damage and neuronal cell death by apoptosis. In addition, epigenetics, including DNA methylation, histone posttranslational modifications (PTMs), and non-coding RNA, play an important role in the neuropathology of FASD. However, little is known about the temporal dynamics and kinetics of histones and their PTMs in FASD. RESULTS: We examined the effects of postnatal alcohol exposure (PAE), an animal model of human third-trimester equivalent, on the kinetics of various histone proteins in two distinct brain regions, the frontal cortex, and the hypothalamus, using in vivo (2)H2O-labeling combined with mass spectrometry-based proteomics. We show that histones have long half-lives that are in the order of days. We also show that H3.3 and H2Az histone variants have faster turnovers than canonical histones and that acetylated histones, in general, have a faster turnover than unmodified and methylated histones. Our work is the first to show that PAE induces a differential reduction in turnover rates of histones in both brain regions studied. These alterations in histone turnover were associated with increased DNA damage and decreased cell proliferation in postnatal rat brain. CONCLUSION: Alterations in histone turnover might interfere with histone deposition and chromatin stability, resulting in deregulated cell-specific gene expression and therefore contribute to the development of the neurological disorders associated with FASD. Using in vivo (2)H2O-labeling and mass spectrometry-based proteomics might help in the understanding of histone turnover following alcohol exposure and could be of great importance in enabling researchers to identify novel targets and/or biomarkers for the prevention and management of fetal alcohol spectrum disorders.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1186/s13148-017-0416-5" target="_blank" rel="noreferrer noopener">10.1186/s13148-017-0416-5</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).
*2H2O-labeling
*Brain
*Genetic Variation
*Histone
*Mass spectrometry
*Post-translational modifications
*Postnatal alcohol exposure
*Turnover
2017
Acetylation
Animal
Animals
Cell Proliferation
Clinical epigenetics
Department of Pharmaceutical Sciences
Disease Models
DNA Damage
Epigenesis
Female
Fetal Alcohol Spectrum Disorders/genetics/*metabolism
Genetic
Histones/*genetics/*metabolism
Humans
Kasumov Takhar
Li Ling
NEOMED College of Pharmacy
Post-Translational
Pregnancy
Previs Stephen
Protein Processing
Proteomics/*methods
Rachdaoui Nadia
Rats
Sarkar Dipak
Sprague-Dawley
Willard Belinda
-
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.111.250126" target="_blank" rel="noreferrer noopener">http://doi.org/10.1161/CIRCRESAHA.111.250126</a>
Pages
241–252
Issue
2
Volume
110
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
Induction of vascular progenitor cells from endothelial cells stimulates coronary collateral growth.
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
2012
2012-01
Subject
The topic of the resource
*Collateral Circulation; *Coronary Circulation; Animal; Animals; Biomarkers/metabolism; Cell Differentiation; Cell Lineage; Cells; Coronary Occlusion/genetics/metabolism/pathology/physiopathology/*surgery; Coronary Vessels/metabolism/pathology/*physiopathology; Cultured; Developmental; Disease Models; Endothelial Cells/metabolism/pathology/*transplantation; Epigenesis; Gene Expression Profiling; Gene Expression Regulation; Genetic; Induced Pluripotent Stem Cells/metabolism/*transplantation; Mice; Muscle; Myocytes; Neovascularization; Physiologic; Rats; Regenerative Medicine/methods; Regional Blood Flow; Reverse Transcriptase Polymerase Chain Reaction; SCID; Smooth; Smooth Muscle/metabolism/pathology/*transplantation; Sprague-Dawley; Teratoma/metabolism/pathology; Time Factors; Transcription Factors/genetics/metabolism; Transduction; Vascular/metabolism/pathology/*physiopathology
Creator
An entity primarily responsible for making the resource
Yin Liya; Ohanyan Vahagn; Pung Yuh Fen; Delucia Angelo; Bailey Erin; Enrick Molly; Stevanov Kelly; Kolz Christopher L; Guarini Giacinta; Chilian William M
Description
An account of the resource
RATIONALE: A well-developed coronary collateral circulation improves the morbidity and mortality of patients following an acute coronary occlusion. Although regenerative medicine has great potential in stimulating vascular growth in the heart, to date there have been mixed results, and the ideal cell type for this therapy has not been resolved. OBJECTIVE: To generate induced vascular progenitor cells (iVPCs) from endothelial cells, which can differentiate into vascular smooth muscle cells (VSMCs) or endothelial cells (ECs), and test their capability to stimulate coronary collateral growth. METHODS AND RESULTS: We reprogrammed rat ECs with the transcription factors Oct4, Klf4, Sox2, and c-Myc. A population of reprogrammed cells was derived that expressed pluripotent markers Oct4, SSEA-1, Rex1, and AP and hemangioblast markers CD133, Flk1, and c-kit. These cells were designated iVPCs because they remained committed to vascular lineage and could differentiate into vascular ECs and VSMCs in vitro. The iVPCs demonstrated better in vitro angiogenic potential (tube network on 2-dimensional culture, tube formation in growth factor reduced Matrigel) than native ECs. The risk of teratoma formation in iVPCs is also reduced in comparison with fully reprogrammed induced pluripotent stem cells (iPSCs). When iVPCs were implanted into myocardium, they engrafted into blood vessels and increased coronary collateral flow (microspheres) and improved cardiac function (echocardiography) better than iPSCs, mesenchymal stem cells, native ECs, and sham treatments. CONCLUSIONS: We conclude that iVPCs, generated by partially reprogramming ECs, are an ideal cell type for cell-based therapy designed to stimulate coronary collateral growth.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1161/CIRCRESAHA.111.250126" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.111.250126</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).
*Collateral Circulation
*Coronary Circulation
2012
Animal
Animals
Bailey Erin
Biomarkers/metabolism
Cell Differentiation
Cell Lineage
Cells
Chilian William M
Circulation research
Coronary Occlusion/genetics/metabolism/pathology/physiopathology/*surgery
Coronary Vessels/metabolism/pathology/*physiopathology
Cultured
Delucia Angelo
Department of Integrative Medical Sciences
Developmental
Disease Models
Endothelial Cells/metabolism/pathology/*transplantation
Enrick Molly
Epigenesis
Gene Expression Profiling
Gene Expression Regulation
Genetic
Guarini Giacinta
Induced Pluripotent Stem Cells/metabolism/*transplantation
Kolz Christopher L
Mice
Muscle
Myocytes
NEOMED College of Medicine
Neovascularization
Ohanyan Vahagn
Physiologic
Pung Yuh Fen
Rats
Regenerative Medicine/methods
Regional Blood Flow
Reverse Transcriptase Polymerase Chain Reaction
SCID
Smooth
Smooth Muscle/metabolism/pathology/*transplantation
Sprague-Dawley
Stevanov Kelly
Teratoma/metabolism/pathology
Time Factors
Transcription Factors/genetics/metabolism
Transduction
Vascular/metabolism/pathology/*physiopathology
Yin Liya