| First Author | Kasai A | Year | 2008 |
| Journal | Arterioscler Thromb Vasc Biol | Volume | 28 |
| Issue | 10 | Pages | 1717-22 |
| PubMed ID | 18599802 | Mgi Jnum | J:159805 |
| Mgi Id | MGI:4452461 | Doi | 10.1161/ATVBAHA.108.163402 |
| Citation | Kasai A, et al. (2008) Retardation of retinal vascular development in apelin-deficient mice. Arterioscler Thromb Vasc Biol 28(10):1717-22 |
| abstractText | 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. |
