| Literature DB >> 28059714 |
Maksim V Plikus1,2, Christian F Guerrero-Juarez2, Mayumi Ito3, Yun Rose Li4, Priya H Dedhia5, Ying Zheng6, Mengle Shao7, Denise L Gay6,8, Raul Ramos2, Tsai-Ching Hsi2, Ji Won Oh2,9, Xiaojie Wang2, Amanda Ramirez2, Sara E Konopelski2, Arijh Elzein2, Anne Wang6, Rarinthip June Supapannachart6, Hye-Lim Lee2, Chae Ho Lim3, Arben Nace6, Amy Guo6, Elsa Treffeisen6, Thomas Andl10, Ricardo N Ramirez2, Rabi Murad2, Stefan Offermanns11, Daniel Metzger12, Pierre Chambon13, Alan D Widgerow14, Tai-Lan Tuan15, Ali Mortazavi2, Rana K Gupta7, Bruce A Hamilton16, Sarah E Millar6, Patrick Seale4,17, Warren S Pear5, Mitchell A Lazar4,18, George Cotsarelis1.
Abstract
Although regeneration through the reprogramming of one cell lineage to another occurs in fish and amphibians, it has not been observed in mammals. We discovered in the mouse that during wound healing, adipocytes regenerate from myofibroblasts, a cell type thought to be differentiated and nonadipogenic. Myofibroblast reprogramming required neogenic hair follicles, which triggered bone morphogenetic protein (BMP) signaling and then activation of adipocyte transcription factors expressed during development. Overexpression of the BMP antagonist Noggin in hair follicles or deletion of the BMP receptor in myofibroblasts prevented adipocyte formation. Adipocytes formed from human keloid fibroblasts either when treated with BMP or when placed with human hair follicles in vitro. Thus, we identify the myofibroblast as a plastic cell type that may be manipulated to treat scars in humans.Entities:
Mesh：
Substances：
Year: 2017 PMID： 28059714 PMCID： PMC5464786 DOI： 10.1126/science.aai8792
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728