Bromodomain-containing protein 7 regulates matrix metabolism and apoptosis in human nucleus pulposus cells through the BRD7-PI3K-YAP1 signaling axis.

摘要: Intervertebral disc degeneration (IDD) results from dysregulated metabolism of the extracellular matrix nucleus pulposus (NP) and involves participation inflammatory factors such as TNF-α. Bromodomain-containing protein 7 (BRD7) shows considerable potential for anti-inflammatory applications. Herein, we investigated role BRD7 in IDD. The immunohistochemistry demonstrated decreased expression severely degenerated human NP tissues compared to those showing mild degeneration. Lentiviruses adenoviruses were used knock down or overexpress YAP1, respectively. Our revealed that knockdown promoted degradation suppressed PI3K YAP1 expression, while overexpression alleviated expression. In addition, inhibition augmented degradation, enhanced apoptosis, reduced whereas synthesis, apoptosis Besides, reversed reductions sulfated glycosaminoglycan levels induced by TNF-α, but this effect was blocked inhibitors. Moreover, shown interact through coimmunoprecipitation analysis. summary, our demonstrate can regulate cells BRD7-PI3K-YAP1 signaling axis. This study might provide new insights into prevention treatment