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- W1864548137 abstract "Background: Fibroblasts exhibit an extraordinary capacity to undergo fibroblast-myofibroblast activation in association with diseases such as pulmonary fibrosis. Little is known regarding the role of mitochondrial function in fibroblast biology in general and phenotypic switching in fibrosis in particular. Aims and objectives: To demonstrate the interplay of mitochondrial metabolism with fibroblast-myofibroblast activation. Methods and Results: We demonstrate that stimulation of primary lung fibroblasts with the profibrotic cytokine TGFβ1 results in an enhanced mitochondrial membrane potential (ΔΨ m ). Moreover, proliferation, ECM deposition, and motility of these cells are increased compared to fibroblasts with lowΔΨ m . Interestingly, TGFβ1-stimulated cells displayed increased expression of profibrotic markers (αSMA, FN1 and Col1), demonstrating fibroblast-myofibroblast activation. To further corroborate these findings, we sorted primary lung fibroblasts for high and low resting ΔΨ m (ΔΨ m H/L). While ΔΨ m H fibroblasts are morphologically indistinguishable, they demonstrate increased myofibroblast activation compared with ΔΨ m L fibroblasts. Finally, total cell homogenates derived from fibrotic, bleomycin-treated mice demonstrated increased ΔΨ m compared with cell homogenates from saline-treated mice. Conclusion: Our data suggest that mitochondrial metabolism plays an important role in the phenotypic activation of lung fibroblasts, both in TGFβ1 stimulated cells in vitro and bleomycin-induced fibrosis in vivo." @default.
- W1864548137 created "2016-06-24" @default.
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- W1864548137 date "2012-09-01" @default.
- W1864548137 modified "2023-09-24" @default.
- W1864548137 title "LSC 2012 abstract - Mitochondrial metabolism controls lung fibroblast activation in vitro and in vivo" @default.
- W1864548137 hasPublicationYear "2012" @default.
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