Human fetal wound healing: a review of molecular and cellular aspects

Abstract

The physiological answer to after birth skin lesions is scarring, which compromises the function and the aesthetics of the injured area. However, fetuses in early gestation (24 weeks or less) respond to this damage with skin regeneration. To explain this difference, several factors are considered, such as increased production of collagen III in fetal fibroblasts and increased presence of this collagen in the skins of these fetuses. Increased hyaluronic acid in fetal matrix correlates with greater capacity for migration of fibroblasts in scarless repair. The fact that myofibroblasts in the wound appear only after the fetal stage of pregnancy which forms scars can also be correlated. Additionally, there is an increase in the amount of adhesion molecules in repair without scarring, which would multiply cell adhesion and migration. Lower levels of bTGF1 in fetal wound are correlated with reduced amounts of collagen I and may be the result of higher relative expression of bTGF3, which downregulates bTGF1. Amniotic fluid itself might be a stimulating factor to human skin's fibroblasts proliferation through cytokines such as bFGF and PDGF. A hypoxic environment in the fetal wound, associated with increased presence of Dot cells in blood, is also observed, and both facts can be related to a difference in the repair of the skin. Distinct gene expression guides those different responses and may also help to elucidate fetal skin regeneration. When the mechanisms responsible for the absence of scars in wounded fetuses are enlightened, it will be a significant mark in the studies of wound cicatrization and its therapeutic applications shall be extremely valuable.