Involvement of ER stress pathway in chronic inflammatory diseases.

2014 Fiscal Year Final Research Report

• Project/Area Number: 23590365
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Pathological medical chemistry
• Research Institution: Kumamoto University
• Principal Investigator: GOTOH TOMOMI 熊本大学, 教育学部, 教授 (20264286)
• Co-Investigator(Renkei-kenkyūsha): OIKE Yuichi 熊本大学, 大学院生命科学研究部, 教授 (90312321) ; ENDO Motoyoshi 熊本大学, 大学院生命科学研究部, 助教 (40398243)
• Project Period (FY): 2011-04-28 – 2015-03-31
• Keywords: 小胞体 / 細胞小器官 / ストレス応答 / アポトーシス / ミトコンドリア / 虚血再灌流障害

Outline of Final Research Achievements

We previously reported that ER stress-CHOP pathway is involved in the formation of atherosclerosis, especially in plaque instability. In this study, we clarified that ER stress-CHOP pathway is involved in the myocardial re-perfusion injury. In this model, we also showed that oxygen radical is involved in the activation of ER stress-CHOP pathway. Treatment with oxygen radical scavenger rescued re-perfusion injury. We also showed that damage of cartilage tissue in OA is mediated by ER stress pathway. Next, we clarified that abnormality of lipid species in ER-Golgi-cell membrane compartment influences mitochondrial function, using SMS1-knock out mice. Recently, it is reported that each organelle stress influence other organelle functions. Therefore, we analyzed a novel putative mitochondrial molecule to clarify the influences on ER in mitochondrial stress. We clarify that putative mitochondrial diseases-related molecule TMEM65 is a mitochondrial inner-membrane protein.

Free Research Field

病態生化学