Cyclophilin B, a molecule chaperone, promotes adipogenesis in 3T3-L1 preadipocytes via AKT/mTOR pathway

Cyclophilin is known to act as a molecular chaperone in the endoplasmic reticulum. Recent studies have reported that the expression of cyclophilin B (CypB) is increased in ob/ob mice and its inhibitor suppresses adipocyte differentiation. However, the mechanism of action of CypB in adipocytes remains to be elucidated. The present study investigated the role of CypB in 3T3-L1 adipocyte differentiation. It showed that the expression level of CypB was increased during 3T3-L1 adipocyte differentiation by reverse transcription-quantitative PCR and western blotting analysis. CypB knockdown using short interfering RNA delayed cell cycle progression from the G(1)/S to G(2)/M phase through the mammalian target of rapamycin (mTOR) signaling pathway and inhibited the expression levels of adipogenic transcription factors including peroxisome proliferator-activated receptor gamma (PPAR gamma) and CCAAT-enhancer binding protein (C/EBP)alpha. Additionally, the accumulation of lipid droplets was inhibited by CypB knockdown. Conversely, overexpression of CypB promoted cell cycle progression from the G(1)/S to G(2)/M phase by the mTOR signaling pathway and enhanced the expression levels of adipogenic transcription factors including PPAR gamma and C/EBP alpha. Finally, the present study showed that CypB downregulated the expression of CHOP, a well-known negative regulator of adipogenesis. Taken together, the data suggested that CypB might serve important physiological regulatory roles in 3T3-L1 adipocyte differentiation.