Impact of endoplasmic reticulum stress on chondrocyte apoptosis in rat model of DDH

Abstract

AbstractDevelopmental dysplasia of the hip (DDH) is a developmental disorder characterized by acetabular dysplasia leading to early osteoarthritis. This study examines the role of endoplasmic reticulum stress (ERS) in chondrocyte apoptosis and cartilage degeneration within a DDH model. In the rat model of DDH, created using a swaddling technique, significant deformities in the femoral head and acetabulum were observed, alongside an upregulation of matrix metalloproteinase‐13 in acetabular cartilage. We also noted increased levels of apoptosis and ERS‐related factors in the acetabular cartilage of DDH models. Additionally, rat chondrocytes exposed to high‐magnitude cyclic tensile strain (CTS, 1 Hz, 10% equibiaxial strain) in vitro exhibited elevated ERS and increased apoptosis. Importantly, treatment with the ERS inhibitor 4‐phenylbutyric acid effectively suppressed apoptosis induced by CTS in chondrocytes. Our findings suggest that ERS contributes to the upregulation of apoptosis‐related factors in chondrocytes within the DDH model, indicating the potential of ERS modulation as a therapeutic approach for DDH‐related cartilage degeneration.