The UCMSC-bFGF/Scaffold System Accelerates the Healing of the Uterine Full-Thickness Injury

Severe uterine injury is a major cause of endometrial scar formation and female infertility. At present, the methods for accelerating injured uterine healing are still lacking. Genetic engineering modification of mesenchymal stem cells (MSCs) has been shown great promise in preclinical studies on regeneration. Here, we constructed a type of umbilical cord MSCs (UC-MSCs) with overexpressed basic fibroblast growth factor (UCMSC-bFGF) and investigated the effects of the UCMSC-bFGF/scaffold on functional regeneration of the full-thickness defect uterus of the rat model. At days 7, 14, and 30 after treatments, the rats were killed and the injured uterus was observed. The structural and functional change of uterine was assessed by hematoxylin and eosin staining, immunohistochemical staining, and fertility experiment. The UCMSC-bFGF/scaffold group exhibited anti-inflammatory effect, and the number of CD45+ cell in the UCMSC-bFGF/scaffold group was significantly less than that in UC-MSCs/scaffold group and scaffold group, but higher than sham-operated group at day 7 postmending. At day 14, the UCMSC-bFGF/scaffold group exhibited dramatically proangiogenesis efficacy compared with UC-MSCs/scaffold group and scaffold group. At day 30, the endometrial thickness, structure of myometrium, and blood vessels in the UCMSC-bFGF/scaffold were better than those of the UC-MSCs/scaffold group and scaffold group, even close to sham-operated group. Implantation rate at injury region postoperation 30 days in the UCMSC-bFGF/scaffold group (8/16) was significantly higher than that in UC-MSCs/scaffold group (1/16) and scaffold group (0/16). Taken together, the UCMSC-bFGF/scaffold system suppressed local inflammation, promoted angiogenesis, and accelerated regeneration of the defected uterine wall, and thereby greatly shortened the healing time of the injured uterus. In this study, we used umbilical cord mesenchymal stem cells (UC-MSCs) with stably overexpressed basic fibroblast growth factor (UCMSC-bFGF) to repair the full-thickness defect uterine wall of the rat model and found that the UCMSC-bFGF/scaffold system suppressed early acute inflammation after uterus injury, promoted angiogenesis, and accelerated regeneration of the injured uterine wall.