The Experiment Research Of Mechanism In Fetal Rats Scarless Wound Healing

Cleft lip and palate is one of the highest incidences of congenital deformities in China. After the surgery repairing, the scar will not only influence the feature but also affect the growthing of maxillary. There is not resultful treatment to reduce the scar. In adults wound healing restores tissue integrity, but the cost is fibrosis and scar. In contrast, the early-gestation fetus has the remarkable ability to heal skin wounds without a scar. This observation was fist reported more than two decades ago and was subsequently confirmed in both animal modes and human fetuses. Since that time, an intensive research effort has focused on unraveling the mechanisms underlying scarless fetal wound repair. Fetal wounds pass from scarless repair to healing with scar formation during gestation. This transition depends on both the size of the wound and the gestational age of the fetus. The mechanism for scarless fetal repair is unknown, but it does not require systemic factors such as the fetal immune system, fetal serum, or amniotic fluid. The cellular gene regulation rather than the external environment is the critical factor in scarless repair.Transforming growth factor-p has been implicated in the ontogenetic transition from scarless fetal repair to adult repair with scar. Fibromodulin can bind and potentially inhibit TGF-P activity. CTGF is present and frequently overexpressed in fibrotic conditions. We hypothesize that TGF-P, CTGF and fibromodulin expression be differentially regulated during the transition from early gestation wounds manifesting scarless fetal-type repair to late gestation wounds manifesting adult-type repair with scar.To investigate the mechanism for scarless fetal repair, skin from fetal Sprague-Dawley rats at time points that represented both the scarless and scar-forming periods of rat gestation was harvested. We analyzed the expression of TGF-pi,-p3, CTGF, and fibromodulin during cutaneous fetal repair by real time PCR. The result suggested that the ontogenetic transition from scarless fetal-type repair to adult-type repair weth scar correlate with the fibromodulin. Fibromodulin may have antifibrotic roles in fetal wound repair. In order to investigate the role of mechanism for fibromodulin in the fetal scarless healing, we constracted the siRNA expression carrier of fibromodulin. After transfected the fibroblast of El 6 and El 8, the fibromodulin's mRNA was effective interfered by analyzed by RT-PCR. The expression of TGF-pi and CTGF increased while the expression of TGF-P3 decreased after the RNA interference of fibromodulin. This suggested that fibromodulin may be a biologically relevant modulator of TGF-p activity and CTGF activity during scarless formation. Relative abundance of fibromodulin in early gestation wounds may partly affect scarless fetal repair through decreased TGF-P and CTGF bioavailability.Base on this foundings, increased fibromodulin induction in fetalwounds offers a novel explanation of fetal wound collagens deposited in a more organized fashion than collagen in adult wounds. Potential strategies for the manipulation of adult wounds into being more "fetal like" may include the addition of fibromodulin to modulate both TGF-p\ CTGF activity and ECM assembly.