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Dynamic regulation of myofibroblast phenotype in cellular senescence
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Dynamic regulation of myofibroblast phenotype in cellular senescence
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Journal Article
Dynamic regulation of myofibroblast phenotype in cellular senescence
2022
Overview
Cellular senescence is an antiproliferative response with a critical role in the control of cellular balance in diverse physiological and pathological settings. Here, we set to study the impact of senescence on the regulation of cell plasticity, focusing on the regulation of the myofibroblastic phenotype in primary fibroblasts. Myofibroblasts are contractile, highly fibrogenic cells with key roles in wound healing and fibrosis. Using cellular models of fibroblast senescence, we find a consistent loss of myofibroblastic markers and functional features upon senescence implementation. This phenotype can be transmitted in a paracrine manner, most likely through soluble secreted factors. A dynamic transcriptomic analysis during paracrine senescence confirmed the non‐cell‐autonomous transmission of this phenotype. Moreover, gene expression data combined with pharmacological and genetic manipulations of the major SASP signaling pathways suggest that the changes in myofibroblast phenotype are mainly mediated by the Notch/TGF‐β axis, involving a dynamic switch in the TGF‐β pathway. Our results reveal a novel link between senescence and myofibroblastic differentiation with potential implications in the physiological and pathological functions of myofibroblasts. Primary fibroblasts under standard tissue culture conditions acquire myofibroblastic features. Cellular senescence results in the loss of myofibroblastic features in these cells. This phenotype can be transmitted by the senescent secretome, and it is associated with a dynamic switch in the TGF‐beta pathway during senescence. These results reveal a link between senescence and myofibroblastic differentiation with potential implications in the physiological and pathological function of myofibroblasts.
Publisher
John Wiley & Sons, Inc,John Wiley and Sons Inc
