differentiation and reprogramming regulated by oxidative stress

• Project/Area Number: 24615001
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Regenerative medicine
• Research Institution: Tohoku University
• Principal Investigator: MORITA Masanobu 東北大学, 医学(系)研究科(研究院), 助教 (10519094)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Project Status: Completed (Fiscal Year 2014)
• Budget Amount: ¥5,590,000 (Direct Cost: ¥4,300,000、Indirect Cost: ¥1,290,000); Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000); Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000); Fiscal Year 2012: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
• Keywords: 幹細胞 / リプログラミング / iPS / 再生医療

Outline of Final Research Achievements

Keap1-Nrf2 system plays pivotal roles in response to oxidative stress. Nrf2 induces anti-oxidant enzymes then reduces oxidative stress in cells, tissues and body.In this study we examined Nrf2 functions in reprogramming process of differentiated cells, in other words, iPS formation. We transfected reprogramming factors Oct3, Sox2, KLF4 and c-Myc into Nrf2 KO MEF and Keap1 KO MEF then counted iPS colonies to judge reprogramming efficiency. Keap1 KO MEF induced less iPS colonies than wild and Nrf2 KO MEF. Gene expression analysis revealed that Nrf2 activated cell cycle arrest factors then induced repression of iPS formation.