Identification of the target molecule to control the intraocular pressure: A study of Vav deficient mice with ocular hypertension

2014 Fiscal Year Final Research Report

• Project/Area Number: 24659755
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Ophthalmology
• Research Institution: Hokkaido University
• Principal Investigator: INOUE Kaoru 北海道大学, 保健科学研究院, 教授 (80133718)
• Co-Investigator(Kenkyū-buntansha): FUJIKAWA Keiko 北海道大学, 大学院保健科学研究院, 客員研究員 (70374246) ; AIHARA Makoto 東京医科歯科大学, 医学部付属病院, 特任教授 (80222462) ; ASAOKA Ryou 東京大学, 医学部付属病院, 講師 (00362202)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 緑内障 / 高眼圧モデル動物 / 遺伝子改変マウス

Outline of Final Research Achievements

We tried to identify the target molecule to control the intraocular pressure (IOP) with Vas-deficient mice, lead to an ocular phenotype. However it failed to identify the specific molecule, because the molecular mechanism of intraocular pressure control is complicated more than our initial assumption.
Therefore we decided first to clarify the relationship between the intraocular pressure and the retinal ganglion cell (RGC) of Vavs-deficient mice. As results, We demonstrate here Vav2,3 KO and Vav2 KO mice show not only the pressure-dependent RGCs death, but also under the normal IOP level, pressure-independent RGC death. It implies that Vav2,3 and Vav2 deficiency in mice may cause RGC death apart from that of pressure insult.

Free Research Field

解剖学