Hypoxia Modulates Fibroblastic Architecture, Adhesion and Migration: A Role for HIF-1 alpha in Cofilin Regulation and Cytoplasmic Actin Distribution
2013 | journal article. A publication with affiliation to the University of Göttingen.
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Hypoxia Modulates Fibroblastic Architecture, Adhesion and Migration: A Role for HIF-1 alpha in Cofilin Regulation and Cytoplasmic Actin Distribution
Vogler, M.; Vogel, S.; Krull, S.; Farhat, K.; Leisering, P.; Lutz, S. & Wuertz, C. M. et al. (2013)
PLoS ONE, 8(7) art. e69128. DOI: https://doi.org/10.1371/journal.pone.0069128
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Details
- Authors
- Vogler, Melanie; Vogel, Sabine; Krull, Sabine; Farhat, Katja; Leisering, Pia; Lutz, Susanne; Wuertz, Christina M.; Katschinski, Doerthe Magdalena; Zieseniss, Anke
- Abstract
- Cells can adapt to hypoxia by various mechanisms. Yet, hypoxia-induced effects on the cytoskeleton-based cell architecture and functions are largely unknown. Here we present a comprehensive analysis of the architecture and function of L929 fibroblasts under hypoxic conditions (1% O-2). Cells cultivated in hypoxia showed striking morphological differences as compared to cells cultivated under normoxic conditions (20% O-2). These changes include an enlargement of cell area and volume, increased numbers of focal contacts and loss of cell polarization. Furthermore the beta- and gamma-actin distribution is greatly altered. These hypoxic adjustments are associated with enhanced cell spreading and a decline of cell motility in wound closure and single cell motility assays. As the hypoxia-inducible factor-1 alpha (HIF-1 alpha) is stabilised in hypoxia and plays a pivotal role in the transcriptional response to changes in oxygen availability we used an shRNA-approach to examine the role of HIF-1 alpha in cytoskeleton-related architecture and functions. We show that the observed increase in cell area, actin filament rearrangement, decrease of single cell migration in hypoxia and the maintenance of p-cofilin levels is dependent on HIF-1 alpha stabilisation.
- Issue Date
- 2013
- Status
- published
- Publisher
- Public Library Science
- Journal
- PLoS ONE
- ISSN
- 1932-6203