Stromal vascular fraction promotes angiogenesis and fat graft survival in mice through the ANG-1/Tie-2 signaling pathway
NI Binting1, HE Yucang1, LI Lei2, XU Jinyu2, LIU Zhaoyang2, LI Liqun1.
1.Department of Plastic Surgery, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325015, China; 2.The Second School of Medicine, Wenzhou Medical University, Wenzhou 325035, China
NI Binting,HE Yucang,LI Lei, et al. Stromal vascular fraction promotes angiogenesis and fat graft survival in mice through the ANG-1/Tie-2 signaling pathway[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2024, 54(4): 266-273.
Abstract：Objective: To investigate the mechanism of new blood vessel formation induced by stromal vascular fragment (SVF) after fat transplantation. Methods: We designed a fat transplantation model of nude mice, and set fat tissue transplantation animal model groups of control group, SVFs group and tyrosine kinase inhibitor (TKI) group. we used these methods of gross weighing, HE staining, Masson staining, Western blot and immunofluorescence staining to detect body mass, pathological manifestations, collagen deposition and protein expression of ANG-1, p-Tie-2, CD31, BAX and BCL-2 in each experimental group and made the statistical analysis to study the effect of SVFs on fat survival. Results: The quality of transplanted objects in SVFs group was significantly higher than that in control group (P<0.001). After TKI administration, the effect of SVFs on the fat mass of grafts was reversed, and the weight of grafts in TKI group was significantly lower than that in SVFs group (P<0.001). The collagen deposition around adipocytes in the SVFs group was significantly reduced, and the adipocytes in the TKI group became fragmented and incomplete. Compared with the control group, the expression levels of ANG-1 and p-Tie-2 in SVFs group were up-regulated, and the expression levels of CD31 protein were significantly increased (P<0.05). After TKI administration, the expression levels of p-Tie-2 and
CD31 protein in TKI group were decreased compared with SVFs group (P<0.05). Compared with the control group, the expression of BAX in SVFs group was decreased and the expression of BCL-2 was increased (P<0.05). The expression of BAX in TKI group was increased and the expression of BCL-2 was decreased that compared with the SVFs group (P<0.05). Conclusion: SVFs can promote angiogenesis and inhibit apoptosis through ANG-1/Tie-2 signaling pathway, thereby improving the survival of transplanted fat.
