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Retardation of retinal vascular development in apelin-deficient mice - PubMed

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. 2008 Oct;28(10):1717-22.

doi: 10.1161/ATVBAHA.108.163402. Epub 2008 Jul 3.

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Retardation of retinal vascular development in apelin-deficient mice

Atsushi Kasai et al. Arterioscler Thromb Vasc Biol. 2008 Oct.

Abstract

Objective: Apelin is an endogenous ligand for the G protein-coupled receptor, APJ, and participates in multiple physiological processes. To identify the roles of endogenous apelin, we investigated the phenotype of apelin-deficient (apelin-KO) mice.

Methods and results: Apelin-KO mice showed impaired retinal vascularization and ocular development, which were analyzed by histology, immunohistochemistry, real-time polymerase chain reaction, and the mouse corneal micropocket assay. Apelin-KO mice showed significantly impaired retinal vascularization in the early postnatal period. Retinal apelin/APJ mRNAs were transiently upregulated during the first 2 postnatal weeks but were undetectable in adults. There were no differences in VEGF or FGF2 mRNA expression, or in the morphology and localization of GFAP-positive astrocytes, in the apelin-KO retinas at P5. The corneal pocket assay showed that angiogenic responses to VEGF and FGF2 were remarkably decreased in apelin-KO mice. The reduced responses to VEGF and FGF2 in apelin-KO mice were partially restored by apelin, but apelin alone did not induce angiogenesis.

Conclusions: Our results suggest that spatiotemporally regulated apelin/APJ signaling participates in retinal vascularization in a cooperative manner with VEGF or FGF2, and contributes to normal ocular development.

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Comment in

  • Apelin-APJ signaling in retinal angiogenesis.

    Kojima Y, Quertermous T. Kojima Y, et al. Arterioscler Thromb Vasc Biol. 2008 Oct;28(10):1687-8. doi: 10.1161/ATVBAHA.108.174847. Arterioscler Thromb Vasc Biol. 2008. PMID: 18799795 Free PMC article. No abstract available.

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