Chyle Fat–Derived Stem Cells Conditioned Medium Inhibits Hypertrophic Scar Fibroblast Activity

CD90型 天狼星红 增生性瘢痕 间充质干细胞 川地34 干细胞 CD44细胞 流式细胞术 医学 细胞生物学 分子生物学 病理 纤维化 体外 免疫学 生物 生物化学
作者
Junnan Chen,Zhihua Li,Zhenya Huang,Liming Liang,Minliang Chen
出处
期刊:Annals of Plastic Surgery [Lippincott Williams & Wilkins]
卷期号:83 (3): 271-277 被引量:16
标识
DOI:10.1097/sap.0000000000001932
摘要

Background Hypertrophic scars (HSs) generally form after injury to the deep layers of the dermis and are characterized by excessive collagen deposition. An increasing amount of evidence has determined that human adipose tissue–derived mesenchymal stem cells attenuate fibrosis in various conditions. We explored the effect and possible mechanism of chyle fat–derived stem cells (CFSCs) on HS formation. Methods Hypertrophic scar–derived fibroblasts (HSFs) and CFSCs were isolated from individual patients. Third-passage CFSCs were isolated and cultured using a mechanical emulsification method, and their surface CD markers were analyzed by flow cytometry. The adipogenic and osteogenic differentiation capacity of the CFSCs was determined using oil red O staining and alizarin red S staining, respectively. Then, the effects of CFSCs on HSFs were assessed in vitro. Hypertrophic scar–derived fibroblasts were treated with starvation-induced conditioned medium from the CFSCs (CFSC-CM). The change in HSF cellular behaviors, such as cell proliferation, migration, and protein expression of scar-related molecules, was evaluated by cell counting assay, scratch wound assay, enzyme-linked immunosorbent assay, and western blotting. All data were analyzed using SPSS 17.0. Results The CFSCs expressed CD90, CD105, and CD73 but did not express CD34, CD45, or CD31. The CFSCs differentiated into adipocytes and osteoblasts under the appropriate induction conditions. Chyle fat–derived stem cells conditioned medium inhibited HSF proliferation and migration. The in vitro and ex vivo studies revealed that CFSC-CM decreased type I collagen, type III collagen, and α smooth muscle actin expression. Conclusions Our results suggest that CFSCs are associated with the inhibition of fibrosis in HSFs by a paracrine effect. The use of CFSC-CM may be a novel therapeutic strategy for HSs.
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