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Arch Gynecol Obstet ; 310(1): 103-111, 2024 Jul.
Article in English | MEDLINE | ID: mdl-38342828

ABSTRACT

OBJECTIVE: Although human umbilical cord-derived mesenchymal stem cells (HU-MSCs) have attracted increasing attention because of their pivotal functions in the process of wound healing, the underlying molecular mechanisms have been poorly understood. It has been shown that the TGF-ß/Smad signaling pathway plays an important role in the process of scar formation. The present study focused on exploring whether HU-MSCs improve uterine incision healing after cesarean delivery in rats via the TGF-ß/Smad signaling pathway. STUDY DESIGN: Pregnant rats were randomly assigned to three groups, including the NP group, incision-injected group (HU-MSCs1 group), and tail vein-injected group (HU-MSCs2 group), and 30 days after cesarean section, sampling was carried out to further explore the specific mechanisms from tissue and protein levels. RESULTS: HU-MSCs secretion could inhibit the fibrosis of scar tissue. We observed that the TGF-ß induced expression of TGF-ß1, Smad2, and Smad3 was attenuated upon HU-MSCs treatment in scar tissue, while the decrease in TGF-ß3 expression was enhanced by HU-MSCs. Furthermore, HU-MSCs treatment accelerated wound healing and attenuated collagen deposition in a damaged uterine rat model, leading to the promoting of uterine incision scarring. In addition, the expression of alpha-smooth muscle actin (a-SMA) was enhanced by HU-MSCs treatment. CONCLUSION: HU-MSCs transplantation promotes rat cesarean section uterine incision scar healing by modulating the TGF-ß/Smad signaling pathway.


Subject(s)
Cesarean Section , Cicatrix , Mesenchymal Stem Cell Transplantation , Mesenchymal Stem Cells , Signal Transduction , Umbilical Cord , Wound Healing , Animals , Female , Mesenchymal Stem Cell Transplantation/methods , Rats , Pregnancy , Umbilical Cord/cytology , Humans , Cicatrix/metabolism , Rats, Sprague-Dawley , Uterus/metabolism , Transforming Growth Factor beta/metabolism , Smad Proteins/metabolism , Transforming Growth Factor beta1/metabolism , Smad3 Protein/metabolism , Smad2 Protein/metabolism
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