β‑catenin signalling inhibits cartilage endplate chondrocyte homeostasis invitro.

Abstract

Cartilaginous endplate degeneration serves a key role in the process of intervertebral disc (IVD) degeneration, however, effective therapies are hindered by an incomplete understanding of the mechanisms that underlie cartilage endplate (CEP) homeostasis and degeneration. Wnt/β-catenin signalling has been reported as a major factor in regulating biological processes. Whether Wnt/β-catenin signalling engages in CEP homeostasis has not yet been investigated. The present study aimed to assess the function of CEP cells via the activation of Wnt/β-catenin signalling to examine and promote the mechanism of degeneration of CEP in vitro. Rat CEP cells were confirmed to exhibit a chondrocytic phenotype by toluidine blue staining. The increased number of senescence-associated β-galactosidase (SA-β-gal)-positive cells and reduced cellular proliferation were investigated in the presence of a β-catenin inhibitor, and the inhibitor improved the trend of senescence. An increased number of apoptotic cells was detected by lithium chloride treatment, and inhibiting Wnt/β-catenin signalling protected the cells from apoptosis. Expression of the catabolic enzymes, metalloproteinase-13 and a disintegrin and metalloproteinase with thrombospondin motifs-5, and the decreased expression of aggrecan were also observed by Wnt/β-catenin signalling activation, and a Wnt/β-catenin signalling inhibitor decreased the expression of catabolic enzymes and increased the expression of aggrecan induced by Wnt/β-catenin signalling activation. Wnt/β-catenin signalling may provide potential strategies for preventing CEP degeneration.