ArticleArthritis research & therapy2019
JAG2/Notch2 inhibits intervertebral disc degeneration by modulating cell proliferation, apoptosis, and extracellular matrix.
Article in Arthritis research & therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 54 citations in OpenAlex.
- THE MICROANATOMY OF INTRACRANIAL HUMAN THROMBI BY SINGLE NUCLEI TRANSCRIPTOMICS.bioRxiv : the preprint server for biology · 2026Article
- Article
- Notch signaling-targeted biomimetic hydrogel constructs an anti-inflammatory "flood-control" system to alleviate pyroptosis for intervertebral disc degeneration treatment.Materials today. Bio · 2026Article
- Fibroblast-Derived Microfibrillar-Associated Protein 5 Exerts Cardioprotective Effects After Myocardial Infarction by Activating the NOTCH2 Signaling in Cardiomyocytes.Journal of the American Heart Association · 2026Article
- Integrative analysis of single-cell RNA sequencing, bulk RNA sequencing, and proteomic data identified NOTCH3 as a hub gene contributing to human intervertebral disc fibrosis.Scientific reports · 2026Article
- Immune cell infiltration and inflammatory response in nucleus pulposus following annular disruption in degenerative disc disease.BMC musculoskeletal disorders · 2025Article
- Mechanism of NOTCH2 in promoting intrahepatic bile duct development.BMC gastroenterology · 2025Article
- Animal Models of Intervertebral Disc Diseases: Advantages, Limitations, and Future Directions.Neurology international · 2024Review
- Article
- Bushen Huoxue Formula Inhibits IL-1β-Induced Apoptosis and Extracellular Matrix Degradation in the Nucleus Pulposus Cells and Improves Intervertebral Disc Degeneration in Rats.Journal of inflammation research · 2024Article
- FOXO3-Activated circFGFBP1 Inhibits Extracellular Matrix Degradation and Nucleus Pulposus Cell Death via miR-9-5p/BMP2 Axis in Intervertebral Disc Degeneration In Vivo and In Vitro.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Engineered extracellular vesicles as therapeutics of degenerative orthopedic diseases.Frontiers in bioengineering and biotechnology · 2023Review
- Whole-transcriptome sequencing identifies key differentially expressed circRNAs/lncRNAs/miRNAs/mRNAs and linked ceRNA networks in adult degenerative scoliosis.Frontiers in molecular neuroscience · 2023Article
- Genomic G-quadruplex folding triggers a cytokine-mediated inflammatory feedback loop to aggravate inflammatory diseases.iScience · 2022Article
- Role of Caspase Family in Intervertebral Disc Degeneration and Its Therapeutic Prospects.Biomolecules · 2022Review
- TNF-α Triggers RIP1/FADD/Caspase-8-Mediated Apoptosis of Astrocytes and RIP3/MLKL-Mediated Necroptosis of Neurons Induced by Angiostrongylus cantonensis Infection.Cellular and molecular neurobiology · 2022Article
- Grem1 accelerates nucleus pulposus cell apoptosis and intervertebral disc degeneration by inhibiting TGF-β-mediated Smad2/3 phosphorylation.Experimental & molecular medicine · 2022Article
- Circular RNA hsa_circ_0083756 promotes intervertebral disc degeneration by sponging miR-558 and regulating TREM1 expression.Cell proliferation · 2022Article
- Notch signaling pathway: architecture, disease, and therapeutics.Signal transduction and targeted therapy · 2022Review
- SKI knockdown suppresses apoptosis and extracellular matrix degradation of nucleus pulposus cells via inhibition of the Wnt/β-catenin pathway and ameliorates disc degeneration.Apoptosis : an international journal on programmed cell death · 2022Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
backgroundIntervertebral disc degeneration (IVDD)-related disorders are the major causes of low back pain. A previous study suggested that Notch activation serves as a protective mechanism and is a part of the compensatory response that maintains the necessary resident nucleus pulposus (NP) cell proliferation to replace lost or non-functional cells. However, the exact mechanism remains to be determined. In this study, we aimed to investigate the role of JAG2/Notch2 in NP cell proliferation and apoptosis.
methodsRecombinant JAG2 or Notch2, Hes1, and Hey2 siRNAs were used to activate or inhibit Notch signaling. Cell proliferation, apoptosis, cell cycle regulatory factors, and pathways associated with Notch-mediated proliferation were examined. In vivo experiments involving an intradiscal injection of Sprague-Dawley rats were performed.
resultsRecombinant JAG2 induced Notch2 and Hes1/Hey2 expression together with NP cell proliferation. Downregulation of Notch2/Hes1/Hey2 induced G0/G1 phase cell cycle arrest in NP cells. Moreover, Notch2 mediated NP cell proliferation by regulating cyclin D1 and by activating PI3K/Akt and Wnt/β-catenin signaling. Furthermore, Notch signaling inhibited TNF-α-promoted NP cell apoptosis by suppressing the formation of the RIP1-FADD-caspase-8 complex. Finally, we found that intradiscal injection of JAG2 alleviated IVDD and that sh-Notch2 aggravated IVDD in a rat model. These results indicated that JAG2/Notch2 inhibited IVDD by modulating cell proliferation, apoptosis, and extracellular matrix. The JAG2/Notch2 axis regulated NP cell proliferation via PI3K/Akt and Wnt/β-catenin signaling and inhibited TNF-α-induced apoptosis by suppressing the formation of the RIP1-FADD-caspase-8 complex.
conclusionsThe current and previous results shed light on the therapeutic implications of targeting the JAG2/Notch2 axis to inhibit or reverse IVDD.
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