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2022 Fiscal Year Final Research Report

Mechanisms of reperfusion of ischemic retina

Research Project

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Project/Area Number 19K09941
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 56060:Ophthalmology-related
Research InstitutionAichi Medical University

Principal Investigator

Kamei Motohiro  愛知医科大学, 医学部, 教授 (40281125)

Project Period (FY) 2019-04-01 – 2023-03-31
Keywords網膜 / 網膜虚血 / 活性化プロテインC / 網膜再灌流 / 網膜アストロサイト / 血管内皮細胞 / ペリサイト
Outline of Final Research Achievements

The results showed that the administration of activated protein C (APC) slowed down the degeneration of astrocytes in the retinal ischemic area compared to the non-treated group.
In a mouse model of oxygen-induced retinopathy (OIR), vessels sprouting from residual vessels extended into the ischemic retina on postnatal day 12, initiating vascular regeneration and forming Neo-Vascular Tufts (NVTs), and individual NVT endothelial cells were coated with pericytes and anti-PDGFRβ antibody was detected on postnatal days 12 and 15 immediately after hyperoxia. Intraperitoneal administration of anti-PDGFRβ antibody at postnatal days 12 and 15, immediately after hyperoxia, and loss of pericytes did not alter the extent of NVTs. Thus, it is clear that endothelial cells autonomously form glomerulosa-like neovessels in the ischemic retina.

Free Research Field

眼科学

Academic Significance and Societal Importance of the Research Achievements

活性型プロテインC(APC)が、虚血網膜における網膜アストロサイトの変性を緩徐にすることが分かった。APCによる実験を継続し、虚血網膜再灌流のメカニズム解明することで、網膜虚血性疾患に対する根治療法を確立すること可能性が高まると考えられる。また、今回虚血網膜において内皮細胞が自律的に糸球体様新生血管を形成することが明らかになり、脈管形成や血管新生の研究にも大きな方向性を示すことができると期待される。

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Published: 2024-01-30  

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