NDLI: Thymosin β4: a key factor for protective effects of eEPCs in acute and chronic ischemia

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Thymosin β4: a key factor for protective effects of eEPCs in acute and chronic ischemia

Content Provider	Scilit
Author	Hinkel, Rabea Bock-Marquette, Ildiko Hazopoulos, Antonis K. Kupatt, Christian
Copyright Year	2010
Description	Journal: Annals of the New York Academy of Sciences Acute myocardial infarction is still one of the leading causes of death in the industrial nations. Even after successful revascularization, myocardial ischemia results in a loss of cardiomyocytes and scar formation. Embryonic EPCs (eEPCs), retroinfused into the ischemic region of the pig heart, provided rapid paracrine benefit to acute and chronic ischemia in a PI‐3K/Akt‐dependent manner. In a model of acute myocardial ischemia, infarct size and loss of regional myocardial function decreased after eEPC application, unless cell pre‐treatment with thymosin β4 shRNA was performed. Thymosin ß4 peptide retroinfusion mimicked the eEPC‐derived improvement of infarct size and myocardial function. In chronic ischemia (rabbit model), eEPCs retroinfused into the ischemic hindlimb enhanced capillary density, collateral growth, and perfusion. Therapeutic neovascularization was absent when thymosin ß4 shRNA was introduced into eEPCs before application. In conclusion, eEPCs are capable of acute and chronic ischemia protection in a thymosin ß4 dependent manner.
Related Links	http://europepmc.org/articles/pmc3601487?pdf=render https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3601487/pdf https://nyaspubs.onlinelibrary.wiley.com/doi/pdf/10.1111/j.1749-6632.2010.05489.x
Ending Page	111
Page Count	7
Starting Page	105
e-ISSN	17496632
DOI	10.1111/j.1749-6632.2010.05489.x
Journal	Annals of the New York Academy of Sciences
Issue Number	1
Volume Number	1194
Language	English
Publisher	Wiley-Blackwell
Publisher Date	2010-05-03
Access Restriction	Open
Subject Keyword	Journal: Annals of the New York Academy of Sciences Cell Tissue Engineering Ischemia/reperfusion
Content Type	Text

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