PDF(Pubmed)
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-β/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-β/Smad signaling pathway.
METHODS: 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-β induced expression of TGF-β1, Smad2, and Smad3 was attenuated upon HU-MSCs treatment in scar tissue, while the decrease in TGF-β3 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.
CONCLUSIONS: HU-MSCs transplantation promotes rat cesarean section uterine incision scar healing by modulating the TGF-β/Smad signaling pathway.
METHODS: 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-β induced expression of TGF-β1, Smad2, and Smad3 was attenuated upon HU-MSCs treatment in scar tissue, while the decrease in TGF-β3 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.
CONCLUSIONS: HU-MSCs transplantation promotes rat cesarean section uterine incision scar healing by modulating the TGF-β/Smad signaling pathway.
摘要：
目的：尽管人脐带间充质干细胞（HU-MSCs）因其在伤口愈合过程中的关键作用而受到越来越多的关注，对潜在的分子机制了解甚少。研究表明,TGF-β/Smad信号通路在瘢痕形成过程中起重要作用。本研究主要探讨HU-MSCs是否通过TGF-β/Smad信号通路促进剖宫产大鼠子宫切口愈合。
方法：妊娠大鼠随机分为三组，包括NP组，切口注射组（HU-MSCs1组），尾静脉注射组（HU-MSCs2组），剖腹产后30天，进行采样以进一步从组织和蛋白质水平探索具体机制。
结果：HU-MSCs分泌可抑制瘢痕组织纤维化。我们观察到TGF-β诱导的TGF-β1，Smad2和Smad3的表达在瘢痕组织中HU-MSCs治疗后减弱，而HU-MSCs增强了TGF-β3表达的降低。此外，HU-MSCs治疗加速受损子宫大鼠模型的伤口愈合并减轻胶原沉积，导致子宫切口瘢痕形成。此外,α-平滑肌肌动蛋白(a-SMA)的表达被HU-MSCs处理增强。
结论：HU-MSCs移植通过调节TGF-β/Smad信号通路促进大鼠剖宫产子宫切口瘢痕愈合。
方法：妊娠大鼠随机分为三组，包括NP组，切口注射组（HU-MSCs1组），尾静脉注射组（HU-MSCs2组），剖腹产后30天，进行采样以进一步从组织和蛋白质水平探索具体机制。
结果：HU-MSCs分泌可抑制瘢痕组织纤维化。我们观察到TGF-β诱导的TGF-β1，Smad2和Smad3的表达在瘢痕组织中HU-MSCs治疗后减弱，而HU-MSCs增强了TGF-β3表达的降低。此外，HU-MSCs治疗加速受损子宫大鼠模型的伤口愈合并减轻胶原沉积，导致子宫切口瘢痕形成。此外,α-平滑肌肌动蛋白(a-SMA)的表达被HU-MSCs处理增强。
结论：HU-MSCs移植通过调节TGF-β/Smad信号通路促进大鼠剖宫产子宫切口瘢痕愈合。
