PDCD4 suppresses autophagy and promotes apoptosis via Akt in chondrocytes of temporomandibular joint osteoarthritis

Objective This study aimed to investigate the role and mechanisms of programmed cell death 4 (PDCD4) in chondrocytes from temporomandibular joint osteoarthritis (TMJOA) rats. Material and Methods Hematoxylin and eosin, Safranin O, and micro-CT were used to detect the morphologic changes in condyles in rat TMJs receiving iodoacetic acid (MIA). The expression of PDCD4, and autophagy- and apoptosis-related proteins in these condyles was measured by immunohistochemistry. Next, using a small interference RNA against PDCD4 (siPDCD4-1086) and/or specific signaling activators, the alteration of PDCD4, and autophagy- and apoptosis-related proteins, as well as Akt and JNK in the IL-1 beta-treated chondrocytes from rat TMJ, was detected by Western blot, immunofluorescence, and flow cytometry, respectively. Results Elevation of PDCD4 and reduction in Beclin1, LC3II, and Bcl2 were observed in OA-like lesions after MIA injection into rat TMJs. Then, PDCD4 downregulated autophagy and promoted apoptosis in the IL-1 beta-treated chondrocytes. Furthermore, Akt, not JNK, was responsible for PDCD4-induced suppressed autophagy and enhanced apoptosis in the IL-1 beta-treated chondrocytes. Conclusion PDCD4 is highly expressed in the rat cartilage of MIA-induced TMJOA and IL-1 beta-treated primary chondrocytes. PDCD4 inhibits autophagy and promotes apoptosis via Akt in these cells.