Version 1
: Received: 4 September 2024 / Approved: 5 September 2024 / Online: 5 September 2024 (11:16:48 CEST)
How to cite:
Chen, S.; Bigdon, S.; Riether, C.; Ma, X.; Niu, X.; Häckel, S.; Li, Z.; Gantenbein, B. The Role of the Bone Morphogenic Protein Agonist Noggin for Nucleus Pulposus Intervertebral Disc Cells. Preprints2024, 2024090399. https://doi.org/10.20944/preprints202409.0399.v1
Chen, S.; Bigdon, S.; Riether, C.; Ma, X.; Niu, X.; Häckel, S.; Li, Z.; Gantenbein, B. The Role of the Bone Morphogenic Protein Agonist Noggin for Nucleus Pulposus Intervertebral Disc Cells. Preprints 2024, 2024090399. https://doi.org/10.20944/preprints202409.0399.v1
Chen, S.; Bigdon, S.; Riether, C.; Ma, X.; Niu, X.; Häckel, S.; Li, Z.; Gantenbein, B. The Role of the Bone Morphogenic Protein Agonist Noggin for Nucleus Pulposus Intervertebral Disc Cells. Preprints2024, 2024090399. https://doi.org/10.20944/preprints202409.0399.v1
APA Style
Chen, S., Bigdon, S., Riether, C., Ma, X., Niu, X., Häckel, S., Li, Z., & Gantenbein, B. (2024). The Role of the Bone Morphogenic Protein Agonist Noggin for Nucleus Pulposus Intervertebral Disc Cells. Preprints. https://doi.org/10.20944/preprints202409.0399.v1
Chicago/Turabian Style
Chen, S., Zhen Li and Benjamin Gantenbein. 2024 "The Role of the Bone Morphogenic Protein Agonist Noggin for Nucleus Pulposus Intervertebral Disc Cells" Preprints. https://doi.org/10.20944/preprints202409.0399.v1
Abstract
Low back pain (LBP) is a significant global health issue, contributing to considerable disability and socioeconomic burdens. The degeneration of the human intervertebral disc (IVD) is a critical factor in the pathogenesis of LBP. Recent studies have emphasized the significance of its specific set of genes and extracellular matrix (ECM) in IVD health. The Noggin gene has emerged as a critical factor due to its high expression levels in healthy nucleus pulposus cells (NPCs) observed in our previous research. In this study, we investigated the hypothesis that decreased Noggin expression in NPCs is associated with IVD degeneration, contributing to LBP development. A lentivirus-mediated RNAi was applied to knockdown Noggin expression in primary NPCs from six human donors. Cell viability analysis, XTT assay, and cell apoptosis were conducted to reveal the effect after transduction. After two weeks, colony formation unit (CFU) assay was used to examine the anchor-independent growth ability of transduced cells. Additionally, qPCR was performed to quantify cellular anabolism and catabolism makers at the transcript level. The results showed lentivirus-mediated downregulation of Noggin suppressed cell growth, cell viability, and colony formation, and induced apoptosis in human NPCs in vitro. Noteworthy, it hindered cellular anabolism and enhanced catabolism activity in human NPCs after transduction. Our findings indicated that the degeneration of human IVD is possibly related to decreased Noggin expression in NPCs. This research provides valuable insights into the role of Noggin in IVD homeostasis and its implications for LBP treatment.
Keywords
Low back pain; Human intervertebral disc; Degeneration; Nucleus pulposus cells; Noggin
Subject
Medicine and Pharmacology, Orthopedics and Sports Medicine
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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