Cx31.1 and cell death in scrape-wounded ‘diabetic’ skin models

Modulating Cx43-mediated communication via gap junctions and/or hemichannels increases skin wound-healing capacity. Cx31.1 expression is associated with apoptosis in eye and ovary. We investigated Cx31.1 and its association with apoptosis in HaCaTs (a human keratinocyte cell line) cultured in normal or ‘diabetic’ levels of glucose and insulin. Cx31.1 protein was increased in high glucose and insulin (HGI) compared to normal glucose and insulin (NGI), and expressed in apoptotic cells. Cx31.1 increased in cells at scrape-wound edges over 48 hours, and caspase was modulated. Scrape-wounded cells caspase activity was higher in HGI (P < 0.05) than NGI. UV exposure increased caspase activity (P < 0.05). In parallel, cell viability was reduced post-UV exposure in NGI treated cells (P < 0.001), although not in HGI. Cx31.1 expression was modulated in HaCaT scrape-wound closure and associated with apoptosis, and ‘diabetic’ conditions. We propose that Cx31.1 is associated with tissue turn-over in diabetic wounds.