The molecular mechanism study of COMP involved in the articular cartilage damage of Kashin-Beck disease.

AIMS

Kashin-Beck disease (KBD) is a kind of chronic osteochondropathy, thought to be caused by environmental risk factors such as T-2 toxin. However, the exact aetiology of KBD remains unclear. In this study, we explored the functional relevance and biological mechanism of cartilage oligosaccharide matrix protein (COMP) in the articular cartilage damage of KBD.

METHODS

The articular cartilage specimens were collected from five KBD patients and five control subjects for cell culture. The messenger RNA (mRNA) and protein expression levels were detected by quantitative reverse transcription PCR (qRT-PCR) and western blot. The survival rate of C28/I2 chondrocyte cell line was detected by MTT assay after T-2 toxin intervention. The cell viability and mRNA expression levels of apoptosis related genes between -overexpression groups and control groups were examined after cell transfection.

RESULTS

The mRNA and protein expression levels of were significantly lower in KBD chondrocytes than control chondrocytes. After the T-2 toxin intervention, the mRNA expression of C28/I2 chondrocyte reduced and the protein level of COMP in three intervention groups was significantly lower than in the control group. MTT assay showed that the survival rate of overexpression KBD chondrocytes were notably higher than in the blank control group. The mRNA expression levels of , , and were also significantly different among COMP overexpression, negative control, and blank control groups.

CONCLUSION

Our study results confirmed the functional relevance of with KBD. may play an important role in the excessive chondrocytes apoptosis of KBD patients.Cite this article: 2020;9(9):578-586.