Bone marrow mesenchymal stem cells promote uterine healing by activating the PI3K/AKT pathway and modulating inflammation in rat models

Figure 5 Bone marrow mesenchymal stromal cells regulate uterine smooth muscle cells through the phosphoinositide 3-kinase/protein kinase B signaling pathway in vitro and in vivo. A: Examination of the impact of bone marrow mesenchymal stromal cells (BMSCs) on phosphorylated phosphoinositide 3-kinase (p-PI3K)/phosphorylated protein kinase B (p-AKT) in uterine wound tissues; B: Comparison of the relative expression levels of p-PI3K/p-AKT in the wound tissues. ^aP < 0.05 vs the natural repair (NR) ; C: Detection of the Kiel67 marker of proliferation (Ki67), p-PI3K, p-AKT, and phosphorylated mechanistic target of rapamycin (p-mTOR) in uterine smooth muscle cells (USMCs) treated with complete culture medium in the presence or absence of 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002), as well as in BMSCs cultured in the presence or absence of LY294002 (25 μM); D: Relative expression levels of Ki67, p-PI3K, p-AKT, and p-mTOR in USMCs under different treatment conditions; E: 5-ethynyl-2’-deoxyuridine assay for assessing the proliferation of USMCs. The treatment was the same as in C (scale bar = 400 μm); F: Percentage of 5-ethynyl-2’-deoxyuridine (EDU)-positive USMCs. The data are presented as mean ± SD, with n = 5 per group for A and n = 3 for C and E. One-way ANOVA was used for multiple comparisons, and a t test was used for comparisons between two groups. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001, ^dP < 0.0001.