scholarly journals Cardiomyocyte‐GSK‐3β deficiency induces cardiac progenitor cell proliferation in the ischemic heart through paracrine mechanisms

2021 ◽  
Author(s):  
Ayesha M. Yusuf ◽  
Rizwan Qaisar ◽  
Abaher O. Al‐Tamimi ◽  
Manju Nidagodu Jayakumar ◽  
James R. Woodgett ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cell ◽  
Ischemic Heart ◽  
Cardiac Progenitor Cell ◽  
Progenitor Cell Proliferation ◽  
Gsk 3Β

scholarly journals CENP-A is essential for cardiac progenitor cell proliferation

Cell Cycle ◽  
2013 ◽  
Vol 13 (5) ◽  
pp. 739-748 ◽  
Author(s):  
Michael McGregor ◽  
Nirmala Hariharan ◽  
Anya Joyo ◽  
Robert L Margolis ◽  
Mark Sussman
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cell ◽  
Cardiac Progenitor Cell ◽  
Progenitor Cell Proliferation

scholarly journals Cardiomyocyte GSK-3β deficiency induces cardiac progenitor cell proliferation in the ischemic heart through paracrine mechanisms

2021 ◽  
Author(s):  
Ayesha M. Yusuf ◽  
Rizwan Qaisar ◽  
Abaher O. Al-Tamimi ◽  
Manju Nidagodu Jayakumar ◽  
James Robert Woodgett ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Growth Factors ◽  
Progenitor Cell ◽  
Glycogen Synthase ◽  
Contractile Function ◽  
Cardiac Regeneration ◽  
Left Ventricular ◽  
Cardiac Progenitor Cell ◽  
Gsk 3Β

Cardiomyopathy is an irreparable loss and novel strategies are needed to induce resident cardiac progenitor cell (CPC) proliferation in situ to enhance the possibility of cardiac regeneration. Here we identify a potential role for glycogen synthase kinase-3β (GSK-3β), a critical regulator of cell proliferation and differentiation, in CPC proliferation that occurs after myocardial infarction (MI). Cardiomyocyte-specific conditional GSK-3β knockout (cKO) and littermate control mice were employed and challenged with MI. Though cardiac left ventricular chamber dimension (LVID) and contractile functions were comparable at two week post-MI, cKO mice displayed significantly preserved LV chamber and contractile function vs. control mice at four-weeks post-MI. Consistent with protective phenotypes, an increased percentage of c-kit positive cells (KPCs) were observed in the cKO hearts at four and six weeks post-MI which was accompanied by increased levels of cardiomyocyte proliferation. Further analysis revealed that the observed increased number of KPCs in the ischemic cKO hearts was mainly from a cardiac lineage as the majority of identified KPCs were negative for the hematopoietic marker, CD45. Mechanistically, cardiomyocyte-GSK-3β profoundly suppresses the expression of growth factors (GFs), including basic-FGF angiopoietin-2, erythropoietin, stem cell factor (SCF), PDGF-BB, G-CSF, and VEGF, post-hypoxia. In conclusion, our findings strongly suggest that loss of cardiomyocyte-GSK-3β promotes cardiomyocyte and resident CPC proliferation post-MI. The induction of cardiomyocytes and CPC proliferation in the ischemic cKO hearts is potentially regulated by autocrine and paracrine signaling governed by dysregulated growth factors post-MI. A strategy to inhibit cardiomyocyte GSK-3β could be helpful for promotion of in-situ cardiac regeneration post-MI injury.

P2X5 purinergic receptor: A novel regulator of human cardiac progenitor cell proliferation and survival

2020 ◽  
Vol 140 ◽  
pp. 13
Author(s):  
Waqas Kayani ◽  
Bingyan Wang ◽  
Kelli Korski ◽  
Alexander Stavropoulos ◽  
Mark Sussman ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cell ◽  
Purinergic Receptor ◽  
Cardiac Progenitor Cell ◽  
Progenitor Cell Proliferation

scholarly journals Abi3bp Regulates Cardiac Progenitor Cell Proliferation and Differentiation

2014 ◽  
Vol 115 (12) ◽  
pp. 1007-1016 ◽  
Author(s):  
Conrad P. Hodgkinson ◽  
Jose A. Gomez ◽  
Alan J. Payne ◽  
Lunan Zhang ◽  
Xiaowen Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Progenitor Cell ◽  
Cardiac Progenitor Cell ◽  
Cell Proliferation And Differentiation ◽  
Proliferation And Differentiation ◽  
Progenitor Cell Proliferation
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