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2015 Fiscal Year Final Research Report

Effect of amiloride on endoplasmic reticulum stress response in the injured spinal cord of rats

Research Project

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Project/Area Number 25462311
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Orthopaedic surgery
Research InstitutionTokai University

Principal Investigator

WATANABE Masahiko  東海大学, 医学部, 教授 (40220925)

Co-Investigator(Kenkyū-buntansha) SUYAMA Kaori  東海大学, 医学部, 助教 (20433914)
Project Period (FY) 2013-04-01 – 2016-03-31
Keywords脊髄損傷 / 小胞体ストレス / オリゴデンドロサイト前駆細胞 / アミロライド
Outline of Final Research Achievements

After spinal cord injury, secondary injury results in an expanding area of glial cell apoptosis. Oligodendrocyte precursor cells (OPC), that are involved in remyelination, have been shown to actively proliferate, but a majority of these cells succumb to apoptosis instead of differentiating into functional oligodendrocytes. In this study, We focused on endoplasmic reticulum (ER) stress as a cause of apoptosis of oligodendrocyte precursor cell following spinal cord injury, and examined it in vivo. We labeled proliferating OPCs and demonstrated that amiloride treatment led to greater numbers of OPCs and also oligodendrocytes in the injured spinal cord. The increased MBP expression suggests that the increased numbers of mature oligodendrocytes led to improved remyelination, which significantly improved motor function recovery.

Free Research Field

整形外科学

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Published: 2017-05-10  

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