Abstract：
:Cutaneous wound healing is accelerated by exogenous mechanical forces and is impaired in TRPC6-knockout mice. Therefore, we designed experiments to determine how mechanical force and TRPC6 channels contribute to wound healing using HaCaT keratinocytes. HaCaT cells were pretreated with hyperforin, a major component of a traditional herbal medicine for wound healing and also a TRPC6 activator, and cultured in an elastic chamber. At 3 h after scratching the confluent cell layer, the ATP release and intracellular Ca(2+) increases in response to stretching (20%) were live-imaged. ATP release was observed only in cells at the frontier facing the scar. The diffusion of released ATP caused intercellular Ca(2+) waves that propagated towards the rear cells in a P2Y-receptor-dependent manner. The Ca(2+) response and wound healing were inhibited by ATP diphosphohydrolase apyrase, the P2Y antagonist suramin, the hemichannel blocker CBX and the TRPC6 inhibitor diC8-PIP2. Finally, the hemichannel-permeable dye calcein was taken up only by ATP-releasing cells. These results suggest that stretch-accelerated wound closure is due to the ATP release through mechanosensitive hemichannels from the foremost cells and the subsequent Ca(2+) waves mediated by P2Y and TRPC6 activation.
journal_name
J Cell Scijournal_title
Journal of cell scienceauthors
Takada H,Furuya K,Sokabe Mdoi
10.1242/jcs.147314subject
Has Abstractpub_date
2014-10-01 00:00:00pages
4159-71issue
Pt 19eissn
0021-9533issn
1477-9137pii
jcs.147314journal_volume
127pub_type
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