Regulation of retinal angiogenesis by endothelial nitric oxide synthase signaling pathway.
10.4196/kjpp.2016.20.5.533
- Author:
Jung Min HA
1
;
Seo Yeon JIN
;
Hye Sun LEE
;
Hwa Kyoung SHIN
;
Dong Hyung LEE
;
Sang Heon SONG
;
Chi Dae KIM
;
Sun Sik BAE
Author Information
1. Gene and Cell Therapy Center for Vessel-Associated Disease, Medical Research Institute, and Department of Pharmacology, Pusan National University School of Medicine, Yangsan 50612, Korea. sunsik@pusan.ac.kr
- Publication Type:Original Article
- Keywords:
Angiogenesis;
eNOS;
Proliferation;
Retina;
Signal transduction
- MeSH:
Animals;
Blood Vessels;
Embryonic Development;
Endothelial Cells;
Female;
Mice;
Muscle, Smooth, Vascular;
Nitric Oxide Synthase Type III*;
Pericytes;
Pregnancy;
Pseudopodia;
Retina;
Retinal Vessels;
Retinaldehyde*;
Signal Transduction
- From:The Korean Journal of Physiology and Pharmacology
2016;20(5):533-538
- CountryRepublic of Korea
- Language:English
-
Abstract:
Angiogenesis plays an essential role in embryo development, tissue repair, inflammatory diseases, and tumor growth. In the present study, we showed that endothelial nitric oxide synthase (eNOS) regulates retinal angiogenesis. Mice that lack eNOS showed growth retardation, and retinal vessel development was significantly delayed. In addition, the number of tip cells and filopodia length were significantly reduced in mice lacking eNOS. Retinal endothelial cell proliferation was significantly blocked in mice lacking eNOS, and EMG-2-induced endothelial cell sprouting was significantly reduced in aortic vessels isolated from eNOS-deficient mice. Finally, pericyte recruitment to endothelial cells and vascular smooth muscle cell coverage to blood vessels were attenuated in mice lacking eNOS. Taken together, we suggest that the endothelial cell function and blood vessel maturation are regulated by eNOS during retinal angiogenesis.
