ArticleJournal of cellular physiology2018
Elevated transforming growth factor β signaling activation in β-actin-knockout mouse embryonic fibroblasts enhances myofibroblast features.
Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
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- Nuclear actin-dependent Meg3 expression suppresses metabolic genes by affecting the chromatin architecture at sites of elevated H3K27 acetylation levels.Nucleic acids research · 2025Article
- Cryoablation-induced modulation of Treg cells and the TGF-β pathway in lung adenocarcinoma: implications for increased antitumor immunity.BMC medicine · 2025Article
- Early events marking lung fibroblast transition to profibrotic state in idiopathic pulmonary fibrosis.Respiratory research · 2023Article
- Green nanotechnology of MGF-AuNPs for immunomodulatory intervention in prostate cancer therapy.Scientific reports · 2021Article
- Loss ofAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2020Article
- Emerging roles of cytoskeletal proteins in regulating gene expression and genome organization during differentiation.Nucleus (Austin, Tex.) · 2020Review
- Elevated transforming growth factor β signaling activation in β-actin-knockout mouse embryonic fibroblasts enhances myofibroblast features.Journal of cellular physiology · 2018Article
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signaling by the transforming growth factor-β (TGF-β) is an essential pathway regulating a variety of cellular events. TGF-β is produced as a latent protein complex and is required to be activated before activating the receptor. The mechanical force at the cell surface is believed to be a mechanism for latent TGF-β activation. Using β-actin null mouse embryonic fibroblasts as a model, in which actin cytoskeleton and cell-surface biophysical features are dramatically altered, we reveal increased TGF-β1 activation and the upregulation of TGF-β target genes. In β-actin null cells, we show evidence that the enhanced TGF-β signaling relies on the active utilization of latent TGF-β1 in the cell culture medium. TGF-β signaling activation contributes to the elevated reactive oxygen species production, which is likely mediated by the upregulation of Nox4. The previously observed myofibroblast phenotype of β-actin null cells is inhibited by TGF-β signaling inhibition, while the expression of actin cytoskeleton genes and angiogenic phenotype are not affected. Together, our study shows a scenario that the alteration of the actin cytoskeleton and the consequent changes in cellular biophysical features lead to changes in cell signaling process such as TGF-β activation, which in turn contributes to the enhanced myofibroblast phenotype.
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Registered trials
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