Exploration of specific biomarkers for carbonyl stress inducible disease.

2014 Fiscal Year Final Research Report

• Project/Area Number: 24390211
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Kidney internal medicine
• Research Institution: Tohoku University
• Principal Investigator: ITO Sadayoshi 東北大学, 医学(系)研究科(研究院), 教授 (40271613)
• Co-Investigator(Kenkyū-buntansha): MORI Takefumi 東北大学, 大学院医学系研究科, 准教授 (40375001) ; NIWANO Yoshimi 東北大学, 大学院歯学研究科, 教授 (40375184) ; SATO Emiko 東北大学, 大学院薬学研究科, 助教 (20466543)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: カルボニルストレス / メチルグリオキサール / 高血圧 / 腎障害 / レニンアンジオテンシン系 / (プロ)レニン受容体 / 免疫応答 / ERK

Outline of Final Research Achievements

Administration of methylglyoxal (MG) to Dahl salt sensitive rats increased blood pressure, renal injury and cardiac-fibrosis. Simultaneously treatment with angiotensin II (AngII) receptor blocker (ARB) ameliorated MG induced blood pressure increase, renal injury and cardiac injury. These results indicate that renin angiotensin system (RAS) partially contribute hypertension and organ injury induced by carbonyl stress.
Since RAS is involved in inflammation, we evaluated the contribution of (pro)renin receptor [(P)RR] to inflammatory reaction. Renin stimulation induced ERK phosphorylation, COX-2 mRNA expression and IL-6 secretion in human peripheral blood mononuclear cells. (P)RR siRNA treatment ameliorated ERK phosphorylation induced by renin stimulation in human leukemic monocyte lymphoma cells. These results indicates that (P)RR could contribute inflammatory response in human inflammatory cells.

Free Research Field

腎臓生理学