Investigation of the mechanisms of intraocular pressure regulation (elevation) by estrogen-receptor

2014 Fiscal Year Final Research Report

• Project/Area Number: 24592621
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Ophthalmology
• Research Institution: University of Yamanashi
• Principal Investigator: MABUCHI Fumihiko 山梨大学, 総合研究部, 講師 (20322125)
• Co-Investigator(Kenkyū-buntansha): AIHARA Makoto 東京医科歯科大学, その他部局等, 教授 (80222462) ; SAKURADA Yoichi 山梨大学, 総合研究部, 助教 (90456476) ; KASHIWAGI Kenji 山梨大学, 総合研究部, 准教授 (30194723) ; IIJIMA Hiroyuki 山梨大学, 総合研究部, 教授 (80114362)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: エストロゲン受容体 / ESR2 / ESR2ノックアウトマウス / 眼圧 / 原発開放隅角緑内障 / POAG

Outline of Final Research Achievements

We previously investigated whether the estrogen receptor beta (ESR2) gene single nucleotide polymorphisms (SNPs) were associated with primary open-angle glaucoma (POAG), and our findings demonstrated a higher frequency of the ESR2 gene SNPs in female patients with POAG in comparison to control subjects, and the maximum intraocular pressure (IOP) in female patients with the risk allele was significantly higher than that in female patients without the risk allele. To elucidate the molecular mechanisms of IOP regulation (elevation) and evaluate the possibility of ESR2 knockout mice as a POAG model, the IOP and optic nerve damage of ESR2 knockout mice were investigated. There was no statistically significant IOP difference (P>0.05) between ESR2 knockout and control (wild type) mice. The retinal thickness and retinal ganglion cells of ESR2 knockout and control mice has been measured and will be counted to evaluate the optic nerve damage.

Free Research Field

緑内障　人類遺伝学