AI Article Synopsis
- Mice embryos have a unique ability to heal wounds without scars up to embryonic day 13 (E13), but this ability decreases after E17, leading to scar formation.
- The protein Lhx2 plays a crucial role in managing hair follicle stem cells during this healing process, with its expression increasing after E13.
- When Lhx2 was knocked down in embryos at E15, wound healing was significantly delayed and scars became more prominent, indicating its importance in both cell division related to healing and the development of scars.
Article Abstract
Multiple transitions occur in the healing ability of the skin during embryonic development in mice. Embryos up to embryonic day 13 (E13) regenerate completely without a scar after full-thickness wounding. Then, up to E16, dermal structures can be formed, including skin appendages such as hair follicles. However, after E17, wound healing becomes incomplete, and scar formation is triggered. Lhx2 regulates the switch between maintenance and activation of hair follicle stem cells, which are involved in wound healing. Therefore, we investigated the role of Lhx2 in fetal wound healing. Embryos of ICR mice were surgically wounded at E13, E15, and E17, and the expression of Lhx2 along with mitotic (Ki67 and p63) and epidermal differentiation (keratin-10 and loricrin) markers was analyzed. The effect of Lhx2 knockdown on wound healing was observed. Lhx2 expression was not noticed in E13 due to the absence of folliculogenesis but was evident in the epidermal basal layer of E15 and E17 and at the base of E17 wounds, along with Ki67 and p63 expression. Furthermore, Lhx2 knockdown in E15 markedly prolonged wound healing and promoted clear scar formation. Therefore, Lhx2 expression is involved in cell division associated with wound healing and may contribute to scar formation in late embryos.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9496086 | PMC |
| http://dx.doi.org/10.3390/biomedicines10092132 | DOI Listing |
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