UNASSIGNED: MSCs from healthy donors were cultured in adipogenesis differentiation medium for 0∼14 days, during which their adipogenesis differentiation degree was evaluated by Oil Red O staining. The expression of IL6R was detected in MSCs during adipogenesis differentiation. Knockdown and overexpression of IL6R were respectively performed using siRNA and lentivirus to investigate its effect on MSCs adipogenesis differentiation. The adipogenesis marker genes expression and MAPK pathway activation were detected by Western blotting. The role of P38 pathway in the adipogenesis differentiation of MSCs was determined using the specific inhibitor SB203580.
UNASSIGNED: The expression of IL6 and IL6R increased during adipogenesis differentiation in MSCs, which were positively correlated with Oil Red O quantification result. Knockdown and overexpression experiments demonstrated a positive correlation between the expressions of IL6R and MSCs adipogenesis differentiation, accompanied by same trend of P38 phosphorylation. Besides, the specific P38 inhibitor SB203580 markedly inhibited the adipogenesis differentiation potential of MSCs.
UNASSIGNED: This study reveals IL6R facilitates the adiogenesis differentiation of MSCs via activating P38 pathway.
■将来自健康供体的MSCs在脂肪生成分化培养基中培养0~14天,在此期间,通过油红O染色评估其脂肪形成分化程度。在骨髓间充质干细胞的脂肪形成分化过程中检测到IL6R的表达。使用siRNA和慢病毒分别进行IL6R的敲低和过表达以研究其对MSCs脂肪生成分化的影响。通过蛋白质印迹法检测脂肪生成标记基因的表达和MAPK途径的激活。使用特异性抑制剂SB203580确定P38途径在MSCs脂肪形成分化中的作用。
■在骨髓间充质干细胞成脂分化过程中IL6和IL6R的表达增加,与油红O定量结果呈正相关。敲低和过表达实验表明IL6R的表达与MSCs的成脂分化呈正相关。伴随着相同的P38磷酸化趋势。此外,特异性P38抑制剂SB203580显著抑制MSCs的成脂分化潜能。
■本研究揭示IL6R通过激活P38途径促进MSCs的脂肪生成分化。