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

Abstract 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‐1β‐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‐1β‐treated chondrocytes. Furthermore, Akt, not JNK, was responsible for PDCD4‐induced suppressed autophagy and enhanced apoptosis in the IL‐1β‐treated chondrocytes. Conclusion PDCD4 is highly expressed in the rat cartilage of MIA‐induced TMJOA and IL‐1β‐treated primary chondrocytes. PDCD4 inhibits autophagy and promotes apoptosis via Akt in these cells.