TGF-β is insufficient to induce adipocyte state loss without concurrent PPARγ downregulation.

ABSTRACT: Cell plasticity, the ability of differentiated cells to convert into other cell types, underlies the pathogenesis of many diseases including the transdifferentiation of adipocytes (fat cells) into myofibroblasts in the pathogenesis of dermal fibrosis. Loss of adipocyte identity is an early step in different types of adipocyte plasticity. In this study, we determine the dynamics of adipocyte state loss in response to the profibrotic cytokine TGF-β. We use two complementary approaches, lineage tracing and live fluorescent microscopy, which both allow for robust quantitative tracking of adipocyte identity loss at the single-cell level. We find that the intracellular TGF-β signaling in adipocytes is inhibited by the transcriptional factor PPARγ, specifically by its ubiquitously expressed isofo

SUBMITTER: Taylor B 

PROVIDER: S-EPMC7442643 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature