Regulation of autophagy in acute kidney injury treatment

2014 Fiscal Year Final Research Report

• Project/Area Number: 23390227
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Single-year Grants
• Section: 一般
• Research Field: Kidney internal medicine
• Research Institution: Kochi University
• Principal Investigator: TERADA Yoshio 高知大学, 教育研究部医療学系, 教授 (30251531)
• Co-Investigator(Kenkyū-buntansha): HORINO Taro 高知大学, 教育研究部医療学系, 講師 (90448382) ; KAGAWA Toru 高知大学, 教育研究部医療学系, 助教 (20380339)
• Project Period (FY): 2011-04-01 – 2015-03-31
• Keywords: 腎臓 / 急性腎障害 / 尿細管 / 再生医学 / 慢性腎臓病 / オートファジー / アポトーシス / 虚血

Outline of Final Research Achievements

Heat shock protein beta-1 (HSPB1, also known as HSP27) is a small heat shock protein that is involved in many cellular processes and reportedly protects cells against oxidative stress. Autophagy is a mechanism that protects cells from many types of stress and is thought to play an important role in preventing stress in acute kidney injury (AKI). We used an in vivo rat ischemia/reperfusion AKI model and cultured renal tubular cells as an in vitro model. To elucidate the regulation of HSPB1, we evaluated the promoter activity and expression of HSPB1 in NRK-52E cells in the presence of H2O2. We showed that HSPB1 expression increased during oxidative stress in AKI. Incremental HSPB1 expression caused autophagy and inhibited apoptosis in renal tubular cells. These results indicate that upregulated HSPB1 plays a role in the pathophysiology of AKI.

Free Research Field

腎臓内科