Thyroid hormone receptor protects against kidney injury by inhibiting tubular cell apoptosis

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K09424
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Endocrinology
• Research Institution: University of Yamanashi
• Principal Investigator: FURUYA Fumihiko 山梨大学, 大学院総合研究部, 講師 (90456450)
• Co-Investigator(Kenkyū-buntansha): 高橋 和也 山梨大学, 大学院総合研究部, 助教 (00646135) ; 北村 健一郎 山梨大学, 大学院総合研究部, 教授 (10304990)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 慢性炎症

Outline of Final Research Achievements

Compared with wild type mice, TR -deficient irradiated chimeric mice showed exacerbated tubulointerstitial injury in the unilateral ureteral obstruction (UUO) model and macrophages isolated from obstructed kidneys of mice lacking TR displayed increased expression of proinflammatory cytokines such as IL-1β. In bone marrow-derived macrophages from wild type mice, T3-depleted culture medium augmented the phosphorylation of IκBα and enhanced the translocation of p65 to the nucleus via a MAPK/MAPK phosphatase pathway. TR -deficient macrophages also increased the release of proinflammatory cytokines that was accompanied by increased nuclear translocation of p65 compared to wild type macrophages. Comparison of TR -deficient bone marrow-derived macrophages with wild-type macrophages confirmed the propensity of these cells to produce exaggerated levels of IL-1β, and their co-culture with renal epithelial cells induced more severe damage to the epithelial cells .

Free Research Field

内分泌学