ABIN‐1 protects chondrocytes from lipopolysaccharide‐induced inflammatory injury through the inactivation of NF‐κB signalling

Abstract

The A20-binding inhibitor of nuclear factor (NF)-κB-1 (ABIN-1) protein has recently been implicated as a key regulator of inflammation with involvement in multiple inflammatory diseases. However, the function of ABIN-1 in osteoarthritis (OA) remains unclear. In the current study, we explored the role of ABIN-1 in the regulation of lipopolysaccharide (LPS)-induced inflammatory injury of chondrocytes, which served as an in vitro model of OA. Results revealed that ABIN-1 expression was induced by chondrocyte exposure to LPS. ABN-1 silencing exacerbated LPS-induced apoptosis and the inflammatory response, while ABIN-1 overexpression alleviated the inflammatory response and LPS-induced apoptosis in chondrocytes. Moreover, ABIN-1 overexpression resulted in significantly decreased LPS-induced NF-κB activation.Notably, activation of NF-κB signalling significantly reversed ABIN-1-mediated inhibitory effects on LPS-induced inflammatory injury in chondrocytes. Taken together, these results demonstrate that ABIN-1 protects chondrocytes against LPS-induced inflammatory injury through the suppression of NF-κB signalling. Our study suggests a potential role for ABIN-1 in OA. Further, we show that ABIN-1 may serve as a potential target for controlling joint inflammation. protects chondrocytes from lipopolysaccharide-induced inflammatory injury through the inactivation of NF-κB signalling.

New Insights into Xenotransplantation for Cartilage Repair: Porcine Multi-Genetically Modified Chondrocytes as a Promising Cell Source

“…Transgenic expression of TNFAIP3 may have an additional therapeutic effect as an inhibitor of the NF-κB-pathway. So far, TNFAIP3mediated NF-κB inhibition in cartilage/chondrocytes has not been directly investigated, but overexpression of ABIN-1, a regulator of TNFAIP3, enabled negative regulation of NF-κB signaling resulting in suppression of apoptosis and maintenance of collagen type II and aggrecan gene expression [49]. In the present study, we could show, that porcine chondrocytes expressing human TNFAIP3 are protected against TNF-and CHX-induced apoptosis.…”

C1q/tumor necrosis factor‐related protein 9 protects cultured chondrocytes from IL‐1β‐induced inflammatory injury by inhibiting NLRP3 inflammasome activation via the AdipoR1/AMPK axis

“…Primary chondrocytes were isolated from mouse articular cartilage following a previously reported experimental method. 22 The isolated chondrocytes were cultured in special culture medium for chondrocytes containing essential nutrients (Procell) for chondrocyte growth. Cells were maintained in an atmosphere containing 5% CO 2 and 95% air at 37 C for growth.…”