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Fibroblast cytoskeletal remodeling induced by tissue stretch involves ATP signaling
Author(s) -
Langevin Helene M.,
Fujita Takumi,
Bouffard Nicole A.,
Takano Takahiro,
Koptiuch Cathryn,
Badger Gary J.,
Nedergaard Maiken
Publication year - 2013
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.24356
Subject(s) - apyrase , pannexin , microbiology and biotechnology , fibroblast , extracellular , ex vivo , purinergic receptor , connexin , cytoskeleton , chemistry , carbenoxolone , biology , gap junction , biochemistry , intracellular , cell , in vitro
Fibroblasts in whole areolar connective tissue respond to static stretching of the tissue by expanding and remodeling their cytoskeleton within minutes both ex vivo and in vivo. This study tested the hypothesis that the mechanism of fibroblast expansion in response to tissue stretch involves extracellular ATP signaling. In response to tissue stretch ex vivo, ATP levels in the bath solution increased significantly, and this increase was sustained for 20 min, returning to baseline at 60 min. No increase in ATP was observed in tissue incubated without stretch or tissue stretched in the presence of the Rho kinase inhibitor Y27632. The increase in fibroblast cross sectional area in response to tissue stretch was blocked by both suramin (a purinergic receptor blocker) and apyrase (an enzyme that selectively degrades extracellular ATP). Furthermore, connexin channel blockers (octanol and carbenoxolone), but not VRAC (fluoxetine) or pannexin (probenecid) channel blockers, inhibited fibroblast expansion. Together, these results support a mechanism in which extracellular ATP signaling via connexin hemichannels mediate the active change in fibroblast shape that occurs in response to a static increase in tissue length. J. Cell. Physiol. 228: 1922–1926, 2013. © 2013 Wiley Periodicals, Inc.