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Disruption of Cell Shape by Serum Withdrawal is Associated With Rapid Downregulation of Transient Receptor Potential Vanilloid 1 (TRPV1) and β‐Tubulin
Author(s) -
Sheth Sandeep,
Jajoo Sarvesh,
Mukherjea Debashree,
Ramkumar Vickram
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.770.8
Subject(s) - trpv1 , protein kinase b , mapk/erk pathway , microbiology and biotechnology , chemistry , downregulation and upregulation , transient receptor potential channel , gene knockdown , p38 mitogen activated protein kinases , pi3k/akt/mtor pathway , cell growth , receptor , signal transduction , apoptosis , endocrinology , biology , biochemistry , gene
Serum deprivation is used as a method for studying the effects of various drugs and growth factors on the cell signaling cascades and gene expression in cultured cells. While studying the effects of growth factors on TRPV1 levels in human embryonic kidney (HEK293) cells stably expressing this receptor, we observed a dramatic disruption of cell shape within 3 h of serum withdrawal. The change in cell shape was time‐dependent, was not associated with apoptosis and was fully restored by serum. No change in cell shape to serum withdrawal was observed in normal untransfected HEK cells. The change in cell shape was partly attenuated by ruthenium red, a nonselective inhibitor of TRPV1, but was unaltered by capsaicin, an agonist of this channel, or by knockdown of TRPV1. Interestingly, serum withdrawal was associated with a rapid loss in the expression of TRPV1 and β‐tubulin and decreased activity of p38 mitogen activated protein kinase (MAPK) and AKT‐1. The decreases in TRPV1 levels were mimicked by inhibition of p38 MAPK but not by AKT‐1, while the decrease in β‐tubulin was dependent on both p‐38 MAPK and AKT‐1. Based on these data, we conclude: 1) the regulation of the levels of TRPV1 and β‐tubulin by serum is essential for cell shape and 2) p38 MAPK and/or AKT‐1 pathways mediate the expression of TRPV1 and β‐tubulin in response to serum. This research was supported by a Central Research Committee grant from SIU School of Medicine.