|  Help  |  About  |  Contact Us

Publication : Retinal vascular leakage occurring in GABA Rho-1 subunit deficient mice.

First Author  Zheng W Year  2010
Journal  Exp Eye Res Volume  90
Issue  5 Pages  634-40
PubMed ID  20193681 Mgi Jnum  J:164143
Mgi Id  MGI:4830809 Doi  10.1016/j.exer.2010.02.012
Citation  Zheng W, et al. (2010) Retinal vascular leakage occurring in GABA Rho-1 subunit deficient mice. Exp Eye Res 90(5):634-40
abstractText  Recent studies demonstrate that GABAergic activity elicits relaxation of retinal arterioles leading to an increase in blood flow. It has also been found that GABAnergic activity in the retina of mice with diabetic retinopathy is suppressed. In this study, we provide further evidence that lack of GABAergic activity significantly alters vasculature development as well as the hypoxia-induced angiogenic response. Using GABA(C) receptor rho(1) subunit-knockout mice (rho-1(-/-)), our results demonstrate that in hypoxia-induced retinas a severe vascular leakage occurred in 2 week-old rho-1(-/-) mice compared with their wildtype counterparts. In addition, our results also showed that all of the rho-1(-/-) mice developed significant retinal vascular leakages by 48 weeks-of-age. Microarray and real-time PCR experiments revealed a unique angiogenesis-related gene expression pattern. This suggests that retinal vascular disorders of rho-1(-/-) mice results from significant up-regulation of angiogenic genes and concomitant down-regulation of anti-angiogenic genes. The study results are consistent with the pathological changes of the retinal vascular leakage seen in diabetic retinopathy. Our data indicate that the GABA(C) rho(1) subunit plays a role in maintaining both homeostasis and balance of retinal neurotransmitter function. Knockout of the retinal GABA(C) rho(1)-subunit leads to changes in vascular permeability similar to the pathological changes induced by retinal hypoxic conditions.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

4 Authors

3 Bio Entities

Trail: Publication

0 Expression