Mechanisms of neuronal-glial-vascular interactions in the retina and the development of novel strategies for treating retinal diseases

2018 Fiscal Year Final Research Report

• Project/Area Number: 16K08554
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General pharmacology
• Research Institution: Yokohama College of Pharmacy
• Principal Investigator: ISHII Kunio 横浜薬科大学, 薬学部, 教授 (90137993)
• Co-Investigator(Kenkyū-buntansha): 中原 努 北里大学, 薬学部, 教授 (10296519) ; 森 麻美 北里大学, 薬学部, 助教 (80453504)
• Project Period (FY): 2016-04-01 – 2019-03-31
• Keywords: 網膜 / 微小循環 / 神経 / グリア細胞 / 血管

Outline of Final Research Achievements

This study aimed to expand and update our current understanding of the mechanisms of neuronal-glial-vascular interactions in the retina, by using the retinal neuronal cell loss model. In the model, the vasculature is impaired by preventing endothelial cell growth and causing capillary regression. We found that 1) astrocytes produce fibronectin, one of extracellular matrices, which provide a scaffold for revascularization, and 2) Muller cells provide vascular growth factors for driving the angiogenesis associated with revascularization, in the retinal neuronal cell loss model. These findings suggest that glial cells (astrocytes and Muller cells) play an important role in the process of the re-vascularization in the injured retina. Manipulation of glial cell function would be a novel strategy for treating retinal diseases.

Free Research Field

医歯薬学

Academic Significance and Societal Importance of the Research Achievements

網膜神経が傷害された際には、一時的に網膜血管への悪影響が認められるが、グリア細胞が神経細胞の役割を補完して、網膜血管の恒常性維持に関与することを明らかにした本研究成果は、網膜における神経-グリア-血管連関のより深い理解をもたらしたとともに、後天性の失明並びに視力低下の主要な原因として、社会問題化している緑内障や網膜症などの網膜疾患に対する治療戦略としてグリア細胞の制御という新しい方向性を示した。