Cx31.1 expression is modulated in HaCaT cells exposed to UV‐induced damage and scrape‐wounding

Louise Nugent, Boatemaa Ofori-Frimpong, Patricia E. Martin, Colin R. Green, Catherine S. Wright*

*Corresponding author for this work

Research output: Contribution to journalArticle

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Abstract

Connexin31.1 (Cx31.1) is a gap junction protein associated with apoptosis. In the skin, apoptosis is modulated by diabetes. A HaCaT skin model investigated whether normal (NGI) and high glucose and insulin (HGI; diabetic) conditions altered Cx31.1 expression, and if these were apoptosis linked. Cx31.1 was found in HaCaT and HeLa Ohio cells, with HaCaT Cx31.1 protein increased in HGI conditions, and around apoptotic cells. HeLa Cx31.1 channels were noncommunicative. Post scrape‐wounding, Cx31.1 increased at wound edges. Caspase 3/7 in scrape‐wounds media (containing cells) elevated in HGI. UV exposure raised Cx31.1, and caspase 3/7, in NGI and HGI. UV reduced cell viability in NGI cells, although not significantly in HGI. Cx31.1 is modulated during HaCaT cell wound closure, and associated with ‘diabetic’ conditions. Cx31.1 expression matched apoptosis levels, higher in HGI cultures. Cx31.1 is noncommunicating, modulated after wounding, linked to apoptosis, and may be associated with tissue turn‐over around diabetic wounds.
Original languageEnglish
JournalJournal of Cellular Physiology
Early online date27 Jun 2020
DOIs
Publication statusE-pub ahead of print - 27 Jun 2020

Keywords

  • Cx31.1
  • apoptosis
  • diabetes
  • gap junctions
  • wound healing

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