Delayed Wound Healing in Keratin 6a Knockout Mice

The study investigated the role of keratin 6a (MK6a) in wound healing by creating MK6a-deficient mice. It was found that MK6a was normally induced in the outer root sheath and interfollicular epidermis upon wounding in wild-type mice, while MK6b was only induced in the suprabasal layers in MK6a-deficient mice. These knockout mice exhibited delayed reepithelialization from hair follicles after superficial wounding, although full-thickness skin wound healing was unaffected. In vitro, MK6a-deficient keratinocytes showed normal migration and proliferation. The findings suggested that MK6a was not crucial for keratinocyte proliferation or migration but played a role in activating follicular keratinocytes post-wounding. This was the first report of a keratin null mutation leading to a wound healing defect.