Contributory role of VEGF overexpression in endothelin-1-induced cardiomyocyte hypertrophy

Nobutake Shimojo, Subrina Jesmin, Sohel Zaedi, Takeshi Otsuki, Seiji Maeda, Naoto Yamaguchi, Kazutaka Aonuma, Yuichi Hattori, Takashi Miyauchi

研究成果: Article査読

34 被引用数 (Scopus)

抄録

Although endothelin-1 (ET-1) stimulates vascular endothelial growth factor (VEGF) expression in a variety of cells, including endothelial cells and vascular smooth muscle cells, the effects of ET-1 on expression of VEGF and its receptors in cardiomyocytes are unknown. In the present study, we found that treatment of neonatal rat cardiomyocytes with ET-1 for 24 h resulted in upregulation of VEGF and its two principal receptors, fetal liver kinase 1 and fms-like tyrosine kinase 1, in a concentration-dependent manner (10 -12 to 10-6 M). ET-1 treatment also caused significant cardiomyocyte hypertrophy, as indicated by increases in cell surface area and [14C]leucine uptake by cardiomyocytes. Treatment with TA-0201 (10-6 M), an ETA-selective blocker, eliminated ET-1-induced overexpression of VEGF and its receptors as well as cardiomyocyte hypertrophy. Treatment with VEGF neutralizing peptides (5-10 μg/ml) partially but significantly inhibited ET-1-induced cardiomyocyte hypertrophy. These results suggest that ET-1 treatment of cardiomyocytes promotes overexpression of VEGF and its receptors via activation of ETA receptors, and consequently the upregulated VEGF signaling system appears to contribute, at least in part, to ET-1-induced cardiomyocyte hypertrophy.

本文言語English
ページ(範囲)H474-H481
ジャーナルAmerican Journal of Physiology - Heart and Circulatory Physiology
293
1
DOI
出版ステータスPublished - 2007 7
外部発表はい

ASJC Scopus subject areas

  • 生理学
  • 循環器および心血管医学
  • 生理学(医学)

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