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Research article
Shi-Qing Feng
Tianjin Medical University General Hospital
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
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.
Methods
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.
Results
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.
Conclusion
Our study suggests that silencing NDC80, RAD21 and BUB1B genes ameliorates intervertebral disc degeneration by promoting proliferation and inhibiting apoptosis of nucleus pulposus cells.
Keywords
Gene silencing, Intervertebral disc degeneration, Nucleus pulposus, Cell cycle, Cell proliferation, Cell apoptosis
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This is a preprint, a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Research article
Shi-Qing Feng
Tianjin Medical University General Hospital
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
History
CURRENT STATUS: Posted
Version 1
Posted 19 Jun, 2020
No community comments so far
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Orthopedics
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background
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.
Methods
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.
Results
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.
Conclusion
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
This is a list of supplementary files associated with this preprint. Click to download.
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