Analysis of mechanism for chondrocyte differentiation and maintenance that overcome cell aging

2016 Fiscal Year Final Research Report

• Project/Area Number: 25293321
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Orthopaedic surgery
• Research Institution: Kyoto University
• Principal Investigator: FUJITA Kaori 京都大学, iPS細胞研究所, 特定研究員 (10633092)
• Co-Investigator(Kenkyū-buntansha): 妻木 範行 京都大学, iPS細胞研究所, 教授 (50303938)
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: 細胞老化 / p53 / p53 isoform / 軟骨細胞分化 / 間葉系幹細胞

Outline of Final Research Achievements

We analyzed that (1) the expression pattern of two isoforms (co-operative p53 β and competitive Δ 133p53) of p53, a major regulator for cellular senescence, in senescence of human mesenchymal stem cells (MSCs) and their ability of differentiation into chondrocytes, and (2) whether overexpression of p53 β in young MSCs induces senescence or overexpression of Δ 133p53 in old (pre-senescent) MSCs inhibits senescence and extends cellular lifespan, and molecular mechanism of their differentiation into chondrocytes. Expression of Δ 133p53, similar results with our previous reports in normal human fibroblasts and normal human CD8 positive T lymphocytes, extended MSC’s lifespan and up regulated the ability of differentiation into chondrocytes. We also found the unique molecular mechanism of Δ 133p53 by metabolome analysis and RNA-sequence, and have studied the detail mechanism.

Free Research Field

分子細胞生物学