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Regeneration of fat cells from myofibroblasts during wound healing
Plikus, Maksim V.,Guerrero-Juarez, Christian F.,Ito, Mayumi,Li, Yun Rose,Dedhia, Priya H.,Zheng, Ying,Shao, Mengle,Gay, Denise L.,Ramos, Raul,Hsi, Tsai-Ching,Oh, Ji Won,Wang, Xiaojie,Ramirez, Amanda,K American Association for the Advancement of Scienc 2017 Science Vol.355 No.6326
<P>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.</P>
Estrogen modulates mesenchyme-epidermis interactions in the adult nipple
Wu, Hsing-Jung,Oh, Ji Won,Spandau, Dan F.,Tholpady, Sunil,Diaz III, Jesus,Schroeder, Laura J.,Offutt, Carlos D.,Glick, Adam B.,Plikus, Maksim V.,Koyama, Sachiko,Foley, John The Company of Biologists 2017 Development (Cambridge) Vol.144 No.8
<P>Maintenance of specialized epidermis requires signals from the underlying mesenchyme; however, the specific pathways involved remain to be identified. By recombining cells from the ventral skin of the K14-PTHrP transgenic mice [which overexpress parathyroid hormone-related protein (PTHrP) in their developing epidermis and mammary glands] with those from wild type, we show that transgenic stroma is sufficient to reprogram wild-type keratinocytes into nipple-like epidermis. To identify candidate nipple-specific signaling factors, we compared gene expression signatures of sorted Pdgfr alpha-positive ventral K14-PTHrP and wild-type fibroblasts, identifying differentially expressed transcripts that are involved in WNT, HGF, TGF beta, IGF, BMP, FGF and estrogen signaling. Considering that some of the growth factor pathways are targets for estrogen regulation, we examined the upstream role of this hormone in maintaining the nipple. Ablation of estrogen signaling through ovariectomy produced nipples with abnormally thin epidermis, and we identified TGF beta as a negatively regulated target of estrogen signaling. Estrogen treatment represses Tgf beta 1 at the transcript and protein levels in K14-PTHrP fibroblasts in vitro, while ovariectomy increases Tgfb1 levels in K14-PTHrP ventral skin. Moreover, ectopic delivery of Tgf beta 1 protein into nipple connective tissue reduced epidermal proliferation. Taken together, these results show that specialized nipple epidermis is maintained by estrogen-induced repression of TGF beta signaling in the local fibroblasts.</P>