Department of Plastic and Reconstructive Surgery, Keio University School of Medicine, Tokyo 160-8582, Japan.
Int J Mol Sci. 2022 Jun 25;23(13):7087. doi: 10.3390/ijms23137087.
Adult mammalian wounds leave visible scars, whereas skin wounds in developing mouse fetuses are scarless until a certain point in development when complete regeneration occurs, including the structure of the dermis and skin appendages. Analysis of the molecular mechanisms at this transition will provide clues for achieving scarless wound healing. The fibroblast growth factor (FGF) family is a key regulator of inflammation and fibrosis during wound healing. We aimed to determine the expression and role of FGF family members in fetal wound healing. ICR mouse fetuses were surgically wounded at embryonic day 13 (E13), E15, and E17. Expression of FGF family members and FGF receptor (FGFR) in tissue samples from these fetuses was evaluated using in situ hybridization and reverse transcription-quantitative polymerase chain reaction. was downregulated in E15 and E17 wounds, and its ligand was upregulated in E13 and downregulated in E15 and E17. Recombinant FGF7 administration in E15 wounds suppressed fibrosis and promoted epithelialization at the wound site. Therefore, the expression level of may correlate with scar formation in late mouse embryos, and external administration of FGF7 may represent a therapeutic option to suppress fibrosis and reduce scarring.
成年哺乳动物的伤口会留下明显的疤痕，而发育中的小鼠胎儿的皮肤伤口在发育的某个特定阶段之前是无疤痕的，此时会发生完全再生，包括真皮和皮肤附属物的结构。分析这一转变过程中的分子机制将为实现无疤痕愈合提供线索。成纤维细胞生长因子 (FGF) 家族是伤口愈合过程中炎症和纤维化的关键调节剂。我们旨在确定 FGF 家族成员在胎儿伤口愈合中的表达和作用。我们通过手术在 E13、E15 和 E17 天的 ICR 胎鼠上造成伤口。使用原位杂交和反转录定量聚合酶链反应评估这些胎鼠组织样本中 FGF 家族成员和 FGF 受体 (FGFR) 的表达。 在 E15 和 E17 伤口中下调，其配体 在 E13 上调，在 E15 和 E17 下调。在 E15 伤口中给予重组 FGF7 可抑制纤维化并促进伤口部位的上皮化。因此， 在晚期小鼠胚胎中的表达水平可能与疤痕形成相关，外源性给予 FGF7 可能是抑制纤维化和减少疤痕形成的治疗选择。
