Role of the ER stress-related molecule ATF6b in a mouse model of multiple sclerosis

2020 Fiscal Year Final Research Report

• Project/Area Number: 18K06500
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 46020:Anatomy and histopathology of nervous system-related
• Research Institution: Kanazawa University
• Principal Investigator: Hori Osamu 金沢大学, 医学系, 教授 (60303947)
• Project Period (FY): 2018-04-01 – 2021-03-31
• Keywords: 小胞体ストレス / 脱髄 / 神経炎症

Outline of Final Research Achievements

It has been reported that endoplasmic reticulum (ER) stress is involved in the pathology of multiple sclerosis and its experimental animal model, EAE. We, therefore, studied the expression and the possible role of ATF6b, an ER stress-related gene, in a mouse EAE model. When EAE was introduced to WT mice, ATF6b was upregulated in both neurons and oligodendrocytes in the spinal cord. Furthermore, when similar experiments were performed with AFT6b KO mice, the paralysis and demyelination was severer than those in WT mice. These results suggest that ATF6b protects neurons and oligodendrocytes in the pathology of EAE.

Free Research Field

神経解剖学

Academic Significance and Societal Importance of the Research Achievements

多発性硬化症は原因不明の中枢性炎症性脱髄疾患である。今回の研究から、小胞体ストレスに関係するATF6bという分子がその病態を制御していることが明らかになった。今後、ATF6bの機能を促進したり、量を増加させたりすることで脱髄が抑制できるのではないかと期待される。