Current address: Department of Molecular Biology and Immunology, National Institute of Agrobiological Sciences, Kannondai 3-1-5, Tsukuba, Ibaraki 305-8602, Japan.
Role of caveolin-1 and cytoskeletal proteins, actin and vimentin, in adipogenesis of bovine intramuscular preadipocyte cells
Article first published online: 2 JAN 2013
© The Author(s) Journal compilation © 2004 International Federation for Cell Biology
Cell Biology International
Volume 28, Issue 8-9, pages 615–623, August 2004
How to Cite
Takenouchi, T., Miyashita, N., Ozutsumi, K., Rose, M. T. and Aso, H. (2004), Role of caveolin-1 and cytoskeletal proteins, actin and vimentin, in adipogenesis of bovine intramuscular preadipocyte cells. Cell Biology International, 28: 615–623. doi: 10.1016/j.cellbi.2004.05.003
- Issue published online: 2 JAN 2013
- Article first published online: 2 JAN 2013
- Received 24 December 2003, revised 27 April 2004, accepted 25 May 2004
We investigated the involvement of caveolin-1 and the cytoskeletal proteins, actin and vimentin, in the adipogenesis of bovine intramuscular preadipocyte (BIP) cells. Immunoblot analysis demonstrated that levels of caveolin-1 and actin gradually increased during adipose conversion in BIP cells, whereas a slight decrease was observed for vimentin. We found that part of the vimentin was clearly distributed to caveolin-1-enriched membrane fractions in BIP cells, but actin was not. During adipogenesis of BIP cells, treatment with the tubulin depolymerizer, nocodazole, significantly increased intracellular triglyceride accumulation compared to non-treated cells. Immunocytochemical analysis showed that actin microfilaments were significantly disrupted in nocodazole-treated cells. Also, a decrease in the localization of vimentin in caveolin-1-enriched fractions and a failure of vimentin to co-immunoisolate with caveolin-1 were observed in nocodazole-treated cells. These results suggest that a rearrangement of cytoskeletal proteins has a role in the intracellular accumulation of lipid droplets during adipogenesis of BIP cells.