Leptin-induced autophagy regulates the immunomodulatory potential of adipose-derived mesenchymal stem cells through down regulating the expression of TSG-6.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Adipose-derived mesenchymal stem cells (ADMSCs) possess modulatory functions in adipose tissue, which could help combat the development of obesity. It has been reported that the functions of ADMSCs are impaired by obese microenvironment. However, the mechanisms are not clearly understood. The study investigates the role of leptin on immunoinhibitory functions of ADMSCs in obesity, and primarily explored its possible mechanisms. ADMSCs were isolated and identified by morphological observation, flow cytometry and differentiation potential. The lipopolysaccharides (LPS)-stimulated macrophages were co-cultured with ADMSCs pretreated with or without leptin. The expression of macrophage-associated markers was detected by flow cytometry. The secretion of inflammatory cytokines was evaluated by ELISA. Autophagy and MAPK signaling related proteins were detected by western blotting. Furthermore, the expression of tumor necrosis factor-alpha-stimulated protein 6 (TSG-6) was detected by western blotting, qRT-PCR, and ELISA. ADMSCs belonged to CD73 + CD90 + CD105 + / CD14 - CD34 - CD45 - HLA-DR - cells, and capable differentiation to adipogenic, osteogenic and chondrogenic cells. The immunosuppressive effect of ADMSCs on macrophage activation were restrained by leptin mediated the expression of TSG-6. Inhibition of leptin induced autophagy by Atg5 knockdown increased the expression of TSG-6

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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