1
40
2
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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
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Bone marrow SSEA1+ cells support the myocardium in cardiac pressure overload.
Publisher
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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
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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
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<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.bmcl.2018.03.061" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.bmcl.2018.03.061</a>
Pages
1937–1942
Issue
10
Volume
28
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
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Novel compounds that target lipoprotein lipase and mediate growth arrest in acute lymphoblastic leukemia.
Publisher
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Bioorganic & medicinal chemistry letters
Date
A point or period of time associated with an event in the lifecycle of the resource
2018
2018-06
Subject
The topic of the resource
*Acute lymphoblastic leukemia; *Cancer; *Co-culture model; *Lipids; *Lipoprotein lipase; *Metabolism; Amides/chemistry/metabolism/pharmacology; Antineoplastic Agents/*chemistry/metabolism/pharmacology; Binding Sites; Cell Line; Cell Proliferation/drug effects; Coculture Techniques; Dyslipidemias/complications/metabolism/pathology; Humans; Lipoprotein Lipase/antagonists & inhibitors/*metabolism; Mesenchymal Stem Cells/cytology/metabolism; Molecular Docking Simulation; Precursor Cell Lymphoblastic Leukemia-Lymphoma/complications/metabolism/pathology; Protein Binding; Protein Structure; Serum Albumin/chemistry/metabolism; Tertiary; Tumor
Creator
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Nair Rajesh R; Geldenhuys Werner J; Piktel Debbie; Sadana Prabodh; Gibson Laura F
Description
An account of the resource
Over the past decade, the therapeutic strategies employed to treat B-precursor acute lymphoblastic leukemia (ALL) have been progressively successful in treating the disease. Unfortunately, the treatment associated dyslipidemia, either acute or chronic, is very prevalent and a cause for decreased quality of life in the surviving patients. To overcome this hurdle, we tested a series of cylopropanecarboxamides, a family demonstrated to target lipid metabolism, for their anti-leukemic activity in ALL. Several of the compounds tested showed anti-proliferative activity, with one, compound 22, inhibiting both Philadelphia chromosome negative REH and Philadelphia chromosome positive SupB15 ALL cell division. The novel advantage of these compounds is the potential synergy with standard chemotherapeutic agents, while concomitantly blunting the emergence of dyslipidemia. Thus, the cylopropanecarboxamides represent a novel class of compounds that can be potentially used in combination with the present standard-of-care to limit treatment associated dyslipidemia in ALL patients.
Identifier
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<a href="http://doi.org/10.1016/j.bmcl.2018.03.061" target="_blank" rel="noreferrer noopener">10.1016/j.bmcl.2018.03.061</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).
*Acute lymphoblastic leukemia
*Cancer
*Co-culture model
*Lipids
*Lipoprotein lipase
*Metabolism
2018
Amides/chemistry/metabolism/pharmacology
Antineoplastic Agents/*chemistry/metabolism/pharmacology
Binding Sites
Bioorganic & medicinal chemistry letters
Cell Line
Cell Proliferation/drug effects
Coculture Techniques
Department of Pharmaceutical Sciences
Department of Pharmacy Practice
Dyslipidemias/complications/metabolism/pathology
Geldenhuys Werner J
Gibson Laura F
Humans
Lipoprotein Lipase/antagonists & inhibitors/*metabolism
Mesenchymal Stem Cells/cytology/metabolism
Molecular Docking Simulation
Nair Rajesh R
NEOMED College of Graduate Studies
NEOMED College of Pharmacy
Piktel Debbie
Precursor Cell Lymphoblastic Leukemia-Lymphoma/complications/metabolism/pathology
Protein Binding
Protein Structure
Sadana Prabodh
Serum Albumin/chemistry/metabolism
Tertiary
Tumor