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Thymosin beta 4 treatment after myocardial infarction does not reprogram epicardial cells into cardiomyocytes.

Abstract：

:Myocardial infarction (MI) is one of the leading causes of morbidity and mortality world-wide. Whether endogenous repair and regenerative ability could be augmented by drug administration is an important issue for generation of novel therapeutic approach. Recently it was reported that in mice pretreated with thymosin beta 4 (TB4) and subsequently subjected to experimental MI, a subset of epicardial cells differentiated into cardiomyocytes. In clinical settings, epicardial priming with TB4 prior to MI is impractical. Here we tested if TB4 treatment after MI could reprogram epicardium into cardiomyocytes and augment the epicardium's injury response. Using epicardium genetic lineage trace line Wt1(CreERT2/+) and double reporter line Rosa26(mTmG/+), we found post-MI TB4 treatment significantly increased the thickness of epicardium and coronary capillary density. However, epicardium-derived cells did not adopt cardiomyocyte fate, nor did they migrate into myocardium to become coronary endothelial cells. Our result thus indicates that TB4 treatment after MI does not alter epicardial cell fate to include the cardiomyocyte lineage, providing both cautions and insights for the full exploration of the potential benefits of TB4 in the clinical settings. This article is part of a Special Issue entitled 'Possible Editorial'.

journal_name

J Mol Cell Cardiol

journal_title

Journal of molecular and cellular cardiology

authors

Zhou B,Honor LB,Ma Q,Oh JH,Lin RZ,Melero-Martin JM,von Gise A,Zhou P,Hu T,He L,Wu KH,Zhang H,Zhang Y,Pu WT

doi

10.1016/j.yjmcc.2011.08.020

subject

Has Abstract

pub_date

2012-01-01 00:00:00

pages

43-7

issue

1

eissn

0022-2828

issn

1095-8584

pii

S0022-2828(11)00340-3

journal_volume

52

pub_type

杂志文章

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