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 G₁/S to G₂/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 γ (PPARγ) and ccAAT-enhancer binding protein (c/EBP)α. Additionally, the accumulation of lipid droplets was inhibited by cypB knockdown. conversely, overexpression of cypB promoted cell cycle progression from the G₁/S to G₂/M phase by the mTOR signaling pathway and enhanced the expression levels of adipogenic transcription factors including PPARγ and c/EBPα. 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.