Interleukin 6 and STAT3 Regulate p63 Isoform Expression in Keratinocytes During Regeneration

The study, conducted 7 years ago, investigated the role of p63, a transcriptional modulator vital to skin development and wound healing, in wound-induced hair follicle neogenesis (WIHN) and its regulation by the IL-6/STAT3 signaling pathway. The researchers used wild type mice and cultured human keratinocytes for the experiments. They found that inhibiting p63 expression by 72% in vivo reduced the number of regenerated hair follicles by approximately 2.5-fold, suggesting that p63 is partially necessary for WIHN in mice. They also found that the IL-6/STAT3 signaling pathway regulates p63 function in human keratinocytes, with IL-6 increasing TAp63 expression and cucurbitacin I, a JAK/STAT3 inhibitor, decreasing it. The study concluded that IL-6/STAT3 activation influences p63 isoform expression in healing wounds and may contribute to WIHN, highlighting the important interaction between immune and developmental signaling pathways during wound healing and regeneration.