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Elevated transforming growth factor signaling activation in -actin-knockout mouse embryonic fibroblasts enhances myofibroblast features
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute. New York University Abu Dhabi (NYUAD), United Arab Emirates.
Number of Authors: 22018 (English)In: Journal of Cellular Physiology, ISSN 0021-9541, E-ISSN 1097-4652, Vol. 233, no 11, p. 8884-8895Article in journal (Refereed) Published
Abstract [en]

Signaling by the transforming growth factor- (TGF-) is an essential pathway regulating a variety of cellular events. TGF- is produced as a latent protein complex and is required to be activated before activating the receptor. The mechanical force at thecell surface is believed to be a mechanism for latent TGF- activation. Using -actin null mouse embryonic fibroblasts as a model, in which actin cytoskeleton and cell-surface biophysical features are dramatically altered, we reveal increased TGF-1 activation and the upregulation of TGF- target genes. In -actin null cells, we show evidence that the enhanced TGF- signaling relies on the active utilization of latent TGF-1 in the cell culture medium. TGF- signaling activation contributes to the elevated reactive oxygen speciesproduction, which is likely mediated by the upregulation of Nox4. The previously observed myofibroblast phenotype of -actin null cells is inhibited by TGF- 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- activation, which in turn contributes to the enhanced myofibroblast phenotype.

Place, publisher, year, edition, pages
2018. Vol. 233, no 11, p. 8884-8895
Keywords [en]
mouse embryonic fibroblast (MEF), myofibroblast, NADPH oxidase 4 (Nox4), reactive oxygen species (ROS), TGF-, -actin
National Category
Biological Sciences
Identifiers
URN: urn:nbn:se:su:diva-162122DOI: 10.1002/jcp.26808ISI: 000446264900045PubMedID: 29851084OAI: oai:DiVA.org:su-162122DiVA, id: diva2:1263074
Available from: 2018-11-14 Created: 2018-11-14 Last updated: 2018-11-14Bibliographically approved

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