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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:1687.)
© 2008 American Heart Association, Inc.

Editorials

Apelin-APJ Signaling in Retinal Angiogenesis

Yoko Kojima; Thomas Quertermous

From the Department of Medicine, Stanford University School of Medicine, Calif.

Correspondence to Thomas Quertermous, MD, Division of Cardiovascular Medicine, Stanford University, 300 Pasteur Drive, Stanford, CA 94305. E-mail tomq1@stanford.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The G protein–coupled receptor (GPCR) APJ (X-msr, angiotensin receptor like 1b) was cloned in several laboratories by homology screening, with the goal of identifying new members of this class of cell surface receptor.¹ This gene attracted attention because of its sequence similarity to the important angiotensin II type 1 receptor and its highly restricted pattern of expression in endothelial cells. Five years later, this GPCR was deorphanized with cloning of the APJ-endogenous ligand apelin. Apelin was found to be synthesized as a 77-aa preproprotein and cleaved to a number of active peptides, including those of 36, 17, and 13 amino acids. Interestingly, apelin was also found to be highly expressed in endothelial cells.

See accompanying article on page 1717

Detailed evaluation of APJ and apelin expression patterns in embryogenesis, and in the developing retina, suggested the hypothesis that autocrine signaling of this pathway in endothelial cells provides a mechanism for regulating new blood vessel growth, or angiogenesis.^2,3 Loss of function experiments in frog embryos using morpholino knockdown experiments have consistently shown vascular developmental abnormalities, varying from perturbed intersomitic vessel branching to more fundamental developmental defects, including loss of the posterior cardinal vein, and decreased numbers of endothelial cells.^2,4 Overexpression of Xapelin led to disorganized expression of endothelial precursor markers at the neurula stage. In zebrafish, knockout studies of one of the APJ homologues (angiotensin receptor like 1b) failed to perturb vascular development, but APJ receptor knockdown was found to decrease . . . [Full Text of this Article]

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Retardation of Retinal Vascular Development in Apelin-Deficient Mice

Atsushi Kasai, Norihito Shintani, Hideaki Kato, Satoshi Matsuda, Fumi Gomi, Ryota Haba, Hitoshi Hashimoto, Michiya Kakuda, Yasuo Tano, and Akemichi Baba
Arterioscler Thromb Vasc Biol 2008 28: 1717-1722. [Abstract] [Full Text] [PDF]