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Cytoskeletal Disassembly and Cell Rounding Promotes Adipogenesis from ES Cells.
- Source :
-
Stem Cell Reviews & Reports . Mar2010, Vol. 6 Issue 1, p74-85. 12p. - Publication Year :
- 2010
-
Abstract
- Biomechanical signals such as cell shape and spreading play an important role in controlling stem cell commitment. Cell shape, adhesion and spreading are also affected by calreticulin, a multifunctional calcium-binding protein, which influences several cellular processes, including adipogenesis. Here we show that cytoskeletal disruption in mouse embryonic stem cells using cytochalasin D or nocodazole promotes adipogenesis. While cytochalasin D disrupts stress fibres and inhibits focal adhesion formation, nocodazole depolymerises microtubules and promotes focal adhesion formation. Furthermore, cytochalasin D increases the levels of both total and activated calcium/calmodulin-dependent protein kinase II, whereas nocodazole decreases it. Nevertheless, both treatments significantly increase the adipogenic potential of embryonic stem cells in vitro. Both cytochalasin D and nocodazole exposure caused cell rounding suggesting that it is cell shape that causes the switch towards the adipogenic programme. Calreticulin-containing embryonic stem cells, under baseline conditions, show low adipogenic potential, have low activity of signalling via calcium/calmodulin-dependent protein kinase II and display normal adhesive properties and cellular spreading in comparison to the highly adipogenic but poorly spread calreticulin-deficient ES cells. We conclude that forced cell rounding via cytoskeletal disruption overrides the effects of calreticulin, an ER chaperone, thus negatively regulating adipogenesis via focal adhesion-mediated cell spreading. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 15508943
- Volume :
- 6
- Issue :
- 1
- Database :
- Academic Search Index
- Journal :
- Stem Cell Reviews & Reports
- Publication Type :
- Academic Journal
- Accession number :
- 52534723
- Full Text :
- https://doi.org/10.1007/s12015-010-9115-8