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2014 Fiscal Year Final Research Report

Angiotensin II type 1 receptor blockade suppresses light-induced neural damage in the mouse retina.

Research Project

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Project/Area Number 24592648
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Ophthalmology
Research InstitutionKeio University

Principal Investigator

KOTO Takashi  慶應義塾大学, 医学部, 講師 (60464814)

Co-Investigator(Kenkyū-buntansha) OZAWA Yoko  慶應義塾大学, 医学部 眼科学教室, 講師 (90265885)
Project Period (FY) 2012-04-01 – 2015-03-31
Keywords網膜 / 光障害 / 神経変性
Outline of Final Research Achievements

We examined the role of angiotensin II type 1 receptor (AT1R) signaling, which is part of the renin-angiotensin system, in light-induced retinal damage. Light-exposed Balb/c mice that were treated with the AT1R blockers (ARBs) before and after the light exposure exhibited attenuated visual function impairment, compared to vehicle-treated mice. Further evaluation of an ARB, valsartan, showed that it suppressed a number of light-induced retinal effects, including thinning of the photoreceptor cell layer caused by apoptosis, shortening of the photoreceptor cell outer segment, and increased levels of reactive oxygen species (ROS). The ARB suppressed the induction of c-fos and the upregulation of fasl after light exposure. Our results suggest that AT1R signaling mediates light-induced apoptosis, by increasing the levels of ROS and proapoptotic molecules in the retina. Thus, AT1R blockade may represent a new therapeutic approach for preventing light-induced retinal neural damage.

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Published: 2016-06-03  

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