Activation of cardiac progenitor cells through paracrine effects of mesenchymal stem cells

被引：107

作者：

Nakanishi, Chiaki ^{[1
,2
]}

Yamagishi, Masakazu ^{[1
]}

Yamahara, Kenichi ^{[2
]}

Hagino, Ikuo ^{[3
]}

Mori, Hidezo ^{[4
]}

Sawa, Yoshiki ^{[5
]}

Yagihara, Toshikatsu ^{[3
]}

Kitamura, Soichiro ^{[3
]}

Nagaya, Noritoshi ^{[2
]}

机构：

[1] Kanazawa Univ, Grad Sch Med, Div Cardiovasc Med, Kanazawa, Ishikawa, Japan

[2] Natl Cardiovasc Ctr, Res Inst, Dept Regenerat Med & Tissue Engn, Osaka 5658565, Japan

[3] Natl Cardiovasc Ctr, Dept Cardiovasc Surg, Osaka, Japan

[4] Natl Cardiovasc Ctr, Dept Cardiac Physiol, Res Inst, Osaka, Japan

[5] Osaka Univ, Dept Surg, Grad Sch Med, Osaka, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2008年 / 374卷 / 01期

关键词：

cardiac progenitor cell; mesenchymal stem cell; paracrine effect; proliferation; migration; differentiation;

D O I：

10.1016/j.bbrc.2008.06.074

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Mesenchymal stem cells (MSC) transplantation has been proved to be promising strategy to treat the failing heart. The effect of MSC transplantation is thought to be mediated mainly in a paracrine manner. Recent reports have suggested that cardiac progenitor cells (CPC) reside in the heart. In this study, we investigated whether MSC had paracrine effects oil CPC in vitro. CPC were isolated from the neonatal rat heart using an explant method. MSC were isolated from the adult rat bone marrow. MSC-derived conditioned medium promoted proliferation of CPC and inhibited apoptosis of CPC induced by hypoxia and serum starvation. Chemotaxis chamber assay demonstrated that MSC-derived conditioned medium enhanced migration of CPC. Furthermore, MSC-derived conditioned medium upregulated expression of cardiomyocyte-related genes in CPC such as beta-myosin heavy chain (beta-MHC) and atrial natriuretic peptide (ANP). In conclusion, MSC-derived conditioned medium had protective effects on CPC and enhanced their migration and differentiation. (C) 2008 Elsevier Inc. All rights reserved.

引用

页码：11 / 16

页数：6

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