IL-17A promotes transdifferentiation of mouse myoblast cells (C2C12) into adipocytes by increasing the expression of peroxisome proliferator-activated receptor gamma through CAAT/enhancer binding protein beta signaling

Abstract

Helper 17 T (Th17) effector cells are a recently identified Th subset and possess a unique property that distinguishes them from Th1 and Th2 subsets. The functional role of Th17 effector cells involves inflammatory responses, including autoimmunity and infection of specific pathogens. Therefore, IL-17A and its receptors may play a key role in determining the progression of certain inflammatory reactions. However, the relationship between IL-17A and adipogenesis has not yet been examined. Therefore, in this study, the effect of IL-17A on the adipogenic transdifferentiation of mouse myoblast (C2C12) cells was examined. CAAT/enhancer binding-protein beta (C/EPB beta) signaling through the IL-17A receptor promoted adipogenic transdifferentiation of myoblast cells by activating peroxisome proliferator-activated receptor gamma (PPAR gamma). These results will advance our understanding of the physiological function of IL-17A in myoblasts during inflammation, as well as the relationship between adipogenesis and inflammation.