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Calcium ion propagation in cultured keratinocytes and other cells in skin in response to hydraulic pressure stimulation
Author(s) -
Goto Makiko,
Ikeyama Kazuyuki,
Tsutsumi Moe,
Denda Sumiko,
Denda Mitsuhiro
Publication year - 2010
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.22121
Subject(s) - calcium , keratinocyte , transient receptor potential channel , calcium in biology , microbiology and biotechnology , stimulation , chemistry , lymphatic endothelium , hydraulic pressure , intracellular , cell culture , biology , endocrinology , biophysics , receptor , immunology , in vitro , lymphatic system , biochemistry , mechanical engineering , genetics , engineering , organic chemistry
We have previously suggested that a variety of environmental factors might be first sensed by epidermal keratinocytes, which represent the frontier of the body. To further examine this idea, in the present study, we examined the intracellular calcium responses of cultured keratinocytes to external hydraulic pressure. First, we compared the responses of undifferentiated and differentiated keratinocytes with those of fibroblasts, vascular endothelial cells (VEC), and lymphatic endothelial cells. Elevation of intracellular calcium was observed after application of pressure to keratinocytes, fibroblasts, and VEC. The calcium propagation extended over a larger area and continued for a longer period of time in differentiated keratinocytes, as compared with the other cells. The response of the keratinocytes was dramatically reduced when the cells were incubated in medium without calcium. Application of a non‐selective transient receptor potential (TRP) channel blocker also attenuated the calcium response. These results suggest that differentiated keratinocytes are sensitive to external pressure and that TRP might be involved in the mechanism of their response. J. Cell. Physiol. 224:229–233, 2010 © 2010 Wiley‐Liss, Inc.