Analyses of gene function for telomere dependent cellular senescence

2015 Fiscal Year Final Research Report

• Project/Area Number: 24590468
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Tokyo Metropolitan Geriatric Hospital and Institute of Gerontology
• Principal Investigator: Ishikawa Naoshi 地方独立行政法人東京都健康長寿医療センター(東京都健康長寿医療センター研究所), 東京都健康長寿医療センター研究所, 研究員 (30184485)
• Co-Investigator(Renkei-kenkyūsha): NAKAMURA Ken-ichi 地方独立行政法人東京都健康長寿医療センター(東京都健康長寿医療センター研究所), 東京都健康長寿医療センター研究所, 研究員 (60159069) ; TAKUBO Kaiyo 地方独立行政法人東京都健康長寿医療センター(東京都健康長寿医療センター研究所), 東京都健康長寿医療センター研究所, 研究部長 研究員 (00154956)
• Project Period (FY): 2012-04-01 – 2016-03-31
• Keywords: テロメア / リプログラミング / ウェルナー症候群 / 加齢 / 線維芽細胞 / 細胞老化 / iPS細胞 / ダウン症

Outline of Final Research Achievements

We have analyzed the in vivo telomere dynamics in Werner syndrome, trisomy 21, and diabetes. Furthermore, our studies of telomere dynamics in patients after living-donor liver transplantation, and in patients with alcoholism and actinic keratosis, have revealed possible factors impacting on telomere maintenance. We also observed end-to-end chromosome fusion in human fibroblast strains at the senescent stage with very short telomeres, and some tumor cells, suggesting that telomere loss could play a role in genetic instability associated with tumorigenesis.
Recently, we analyzed details of the telomere dynamics in iPS cells, indicating that telomere has been lengthen or well maintained during reprograming process. The telomeres of some iPS cell strains became shorter as passages increased without differentiation induction, and those strains showed chromosomal abnormalities. The data suggested that telomere shortening could be a novel marker of iPS cell quality.

Free Research Field

分子病理学