title: Inhibition of the integrin signal constitutes a mouse iPS cell niche.
abstract: Stem cells are regulated by their surrounding microenvironments, called niche, such as cell-cell interaction and extracellular matrix. Classically, feeder cells as a niche have been used in the culture of iPS cells from both the mouse and the human. However, the regulation mechanism of stem cells by feeder cells as a niche still have been partially unclear. In this study, we used three murine iPS cell lines, iPS-MEF-Ng-20D-17, iPS-MEF-Ng-178B-5 and iPS-MEF-Fb/Ng-440A-3, which were generated by different reprogramming methods. In general, these cell lines commonly need the feeder cells as a niche to culture. Recently, the effect of substrate stiffness is known in stem cell study. First, we focused on the mechanical properties of feeder cells, and then we speculated that feeder-less culture might be made possible by using molecules in place of the mechanical properties of the niche. Finally, we found that the combination of disintegrin (echistatin) and 2i (GSK3 inhibitor and MEK inhibitor) is a sufficient condition for three murine iPS culture. This novel method of mimicking the murine iPS cell niche may be useful to understand signaling pathways to maintain the pluripotency of stem cells.
authors.affiliation: Tokyo Women's Medical University Institute for Integrated Medical Sciences, Tokyo, 162-8666, Japan.
authors.forename: Sayaka
authors.initials: S
authors.lastname: Higuchi
authors.affiliation: Department of Physiology, Tokyo Women's Medical University School of Medicine, Tokyo, 162-8666, Japan.
authors.forename: Sawako
authors.initials: S
authors.lastname: Yoshina
authors.affiliation: Tokyo Women's Medical University Institute for Integrated Medical Sciences, Tokyo, 162-8666, Japan. mitani.shohei@twmu.ac.jp.|Department of Physiology, Tokyo Women's Medical University School of Medicine, Tokyo, 162-8666, Japan. mitani.shohei@twmu.ac.jp.
authors.forename: Shohei
authors.initials: S
authors.lastname: Mitani
mesh_terms: D000818:Animals; D002450:Cell Communication / Q000187:drug effects; D018929:Cell Culture Techniques; D002454:Cell Differentiation; D002478:Cells, Cultured; D065150:Cellular Reprogramming; D038362:Glycogen Synthase Kinase 3 / Q000037:antagonists & inhibitors; D057026:Induced Pluripotent Stem Cells / Q000187:drug effects / Q000502:physiology*; D016023:Integrins / Q000037:antagonists & inhibitors* / Q000378:metabolism; D036341:Intercellular Signaling Peptides and Proteins; D020930:MAP Kinase Kinase Kinases / Q000037:antagonists & inhibitors; D051379:Mice; D000066450:Mouse Embryonic Stem Cells / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D010455:Peptides / Q000494:pharmacology; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D015398:Signal Transduction / Q000187:drug effects; D055153:Stem Cell Niche / Q000187:drug effects / Q000502:physiology*
chemical_list: D016023:Integrins; D036341:Intercellular Signaling Peptides and Proteins; D010455:Peptides; D047428:Protein Kinase Inhibitors; C057986:echistatin; D020930:MAP Kinase Kinase Kinases; D038362:Glycogen Synthase Kinase 3
keywords: 2i; disintegrin; feeder-less; miPSC; niche