期刊
ANGIOGENESIS
卷 15, 期 3, 页码 349-360出版社
SPRINGER
DOI: 10.1007/s10456-012-9265-1
关键词
Heart development; Angiogenesis; Nucleotides; Endothelial cells; P2Y receptors
资金
- Action de Recherche Concertee of the Communaute Francaise de Belgique
- Politique Scientifique Federale [IAP-P6/30]
- Prime Minister's Office
- Federal Service for Science, Technology and Culture
- Fonds de la Recherche Scientifique Medicale (F.R.S.M.)
- Fonds d'Encouragement a la Recherche (F.E.R.)
- Fonds Emile DEFAY
- Fonds de la Recherche Scientifique Medicale of Belgium
- Walloon Region (Programme d'Excellence CIBLES)
- European Community [LSHB-2003-503337]
- Fonds National de la Recherche Scientifique/FRIA, Belgium
- Fonds pour la Chirurgie Cardiaque
- F.S.R. (Fonds Special de Recherche) of the U.C.L. (Universite catholique de Louvain)
Communication between endothelial cells and cardiomyocytes is critical for cardiac development and regeneration. However the mechanisms involved in these endothelial-cardiomyocyte interactions remain poorly understood. Nucleotides are released within the heart, especially under ischemia or pressure overload. The function of P2Y nucleotide receptors in cardiac development has never been investigated. Here we show that adult P2Y(4)-null mice display microcardia. P2Y(4) nucleotide receptor is expressed in cardiac endothelial cells but not in cardiomyocytes. Loss of P2Y(4) in cardiac endothelial cells strongly inhibits their growth, migration and PDGF-B secretion in response to UTP. Proliferation of microvessels and cardiomyocytes is reduced in P2Y(4)-null hearts early after birth, resulting in reduced heart growth. Our study uncovers mouse P2Y(4) receptor as an essential regulator of cardiac endothelial cell function, and illustrates the involvement of endothelial-cardiomyocyte interactions in post-natal heart development. We also detected P2Y(4) expression in human cardiac microvessels. P2Y(4) receptor could constitute a therapeutic target to regulate cardiac remodelling and post-ischemic revascularisation.
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