Carbonic Anhydrase VI in Skin Wound Healing Study on <i>Car6</i> Knockout Mice

• Main Authors: Toini Pemmari, Jaakko Laakso, Maarit S. Patrikainen, Seppo Parkkila, Tero A. H. Järvinen
• Format: Article
• Language: English
• Published: MDPI AG 2020-07-01
• Series: International Journal of Molecular Sciences
• Subjects: carbonic anhydrase 6; neural growth factor; saliva; breast milk; skin wound; re-epithelization
• Online Access: https://www.mdpi.com/1422-0067/21/14/5092

Carbonic anhydrases (CAs) contribute to tumor cell migration by generating an acidic environment through the conversion of carbon dioxide to bicarbonate and a proton. CA VI is secreted to milk and saliva, and it could contribute to wound closure, as a potential trophic factor, in animals that typically lick their wounds. Our aim was to investigate whether human CA VI improves skin-wound healing in full-thickness skin-wound models. The effect was studied in <i>Car6</i> ^−/− knockout mice and wild type littermates. Half of both mice strains were given topically administered, milk-derived CA VI after wounding and eight hours later. The amount of topically given CA VI exceeded the predicted amount of natural saliva-delivered CA VI. The healing was followed for seven days and studied from photographs and histological sections. Our results showed no significant differences between the treatment groups in wound closure, re-epithelization, or granulation tissue formation, nor did the <i>Car6</i> genotype affect the healing. Our results demonstrate that CA VI does not play a major role in skin-wound healing and also suggest that saliva-derived CA VI is not responsible for the licking-associated improved wound healing in animals.