Silencing NDC80, RAD21 and BUB1B ameliorates intervertebral disc degeneration by promoting proliferation and inhibiting apoptosis of nucleus pulposus cells
Intervertebral disc degeneration (IVDD) is a commonly occurring musculoskeletal disorder, which is closely associated with low back pain. Accumulating evidence has demonstrated that dysregulated genes expression profiles play important roles in pathogenesis of IVDD. Hence, the current study was aimed to identify key genes to understand underlying mechanisms and therapeutic targets of IVDD.
Microarray datasets of GSE34095, GSE63492 and GSE45856 were downloaded to identify the hub genes that participate in the IVDD pathogenesis. After establishment of rat IVDD models, the expressions of NDC80, BUB1B and RAD21 in rat IVDD samples were evaluated by reverse transcription quantitative PCR (RT-qPCR) and immunochemistry. Subsequently, we assessed the proliferation, cycle and apoptosis of nucleus pulposus (NP) cells that transfected with siRNA-NDC80, siRNA-BUB1B and siRNA-RAD21.
Our results showed indicated that NDC80, BUB1B and RAD21 were the key pathogenic genes with higher expression in IVDD rats, and silencing of NDC80, BUB1B and RAD21 gene could promote the aggrecan and collagen II synthesis, cell cycle and proliferation of NP cells, and inhibit NP cells apoptosis.
Our study suggests that silencing NDC80, RAD21 and BUB1B genes ameliorates intervertebral disc degeneration by promoting proliferation and inhibiting apoptosis of nucleus pulposus cells.
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Posted 19 Jun, 2020
Silencing NDC80, RAD21 and BUB1B ameliorates intervertebral disc degeneration by promoting proliferation and inhibiting apoptosis of nucleus pulposus cells
Posted 19 Jun, 2020
Intervertebral disc degeneration (IVDD) is a commonly occurring musculoskeletal disorder, which is closely associated with low back pain. Accumulating evidence has demonstrated that dysregulated genes expression profiles play important roles in pathogenesis of IVDD. Hence, the current study was aimed to identify key genes to understand underlying mechanisms and therapeutic targets of IVDD.
Microarray datasets of GSE34095, GSE63492 and GSE45856 were downloaded to identify the hub genes that participate in the IVDD pathogenesis. After establishment of rat IVDD models, the expressions of NDC80, BUB1B and RAD21 in rat IVDD samples were evaluated by reverse transcription quantitative PCR (RT-qPCR) and immunochemistry. Subsequently, we assessed the proliferation, cycle and apoptosis of nucleus pulposus (NP) cells that transfected with siRNA-NDC80, siRNA-BUB1B and siRNA-RAD21.
Our results showed indicated that NDC80, BUB1B and RAD21 were the key pathogenic genes with higher expression in IVDD rats, and silencing of NDC80, BUB1B and RAD21 gene could promote the aggrecan and collagen II synthesis, cell cycle and proliferation of NP cells, and inhibit NP cells apoptosis.
Our study suggests that silencing NDC80, RAD21 and BUB1B genes ameliorates intervertebral disc degeneration by promoting proliferation and inhibiting apoptosis of nucleus pulposus cells.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5