Interferon regulatory factor 6 is required for proper wound healing in vivo.

ABSTRACT:

Background

Van der Woude syndrome (VWS) is the most common form of syndromic orofacial cleft caused predominantly by mutations in Interferon Regulatory Factor 6 (IRF6). We previously reported that individuals with VWS have increased risk of wound healing complications following cleft repair compared with individuals with nonsyndromic orofacial clefts (nonsyndromic cleft lip and palate-NSCLP). In vitro, absence of IRF6 leads to impaired keratinocyte migration and embryonic wound healing. However, there is currently no data on tissue repair in adult animals and cells with reduced levels of IRF6 like in VWS.

Results

Excisional wounds of Irf6^+/- and wild-type animals were analyzed 4 and 7 days post-wounding. Although all wounds were reepithelialized after 7 days, the

SUBMITTER: Rhea L 

PROVIDER: S-EPMC9266192 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature