Cardiac Fibroblasts Regulate Myocardial Proliferation through β1 Integrin Signaling

Masaki Ieda, Takatoshi Tsuchihashi, Kathryn N. Ivey, Robert S. Ross, Ting Ting Hong, Robin M. Shaw, Deepak Srivastava

研究成果: Article査読

419 被引用数 (Scopus)

抄録

Growth and expansion of ventricular chambers is essential during heart development and is achieved by proliferation of cardiac progenitors. Adult cardiomyocytes, by contrast, achieve growth through hypertrophy rather than hyperplasia. Although epicardial-derived signals may contribute to the proliferative process in myocytes, the factors and cell types responsible for development of the ventricular myocardial thickness are unclear. Using a coculture system, we found that embryonic cardiac fibroblasts induced proliferation of cardiomyocytes, in contrast to adult cardiac fibroblasts that promoted myocyte hypertrophy. We identified fibronectin, collagen, and heparin-binding EGF-like growth factor as embryonic cardiac fibroblast-specific signals that collaboratively promoted cardiomyocyte proliferation in a paracrine fashion. Myocardial β1-integrin was required for this proliferative response, and ventricular cardiomyocyte-specific deletion of β1-integrin in mice resulted in reduced myocardial proliferation and impaired ventricular compaction. These findings reveal a previously unrecognized paracrine function of embryonic cardiac fibroblasts in regulating cardiomyocyte proliferation.

本文言語English
ページ(範囲)233-244
ページ数12
ジャーナルDevelopmental Cell
16
2
DOI
出版ステータスPublished - 2009 2月 17
外部発表はい

ASJC Scopus subject areas

  • 分子生物学
  • 生化学、遺伝学、分子生物学(全般)
  • 発生生物学
  • 細胞生物学

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