ArticleArthritis research & therapy2008
Synergistic role of c-Myc and ERK1/2 in the mitogenic response to TGF beta-1 in cultured rat nucleus pulposus cells.
Article in Arthritis research & therapy, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Role of macrophage in intervertebral disc degeneration.Bone research · 2025Review
- Unveiling the Promising Role of Substance P/Neurokinin 1 Receptor in Cancer Cell Proliferation and Cell Cycle Regulation in Human Malignancies.Current medicinal chemistry · 2025Review
- Investigating the Effects of Chordoma Cell-Derived Exosomes on the Tumorigenicity of Nucleus Pulposus Cells.Journal of neurological surgery. Part B, Skull base · 2024Article
- Progress in regulating inflammatory biomaterials for intervertebral disc regeneration.Bioactive materials · 2024Review
- Intervertebral disc cell fate during aging and degeneration: apoptosis, senescence, and autophagy.North American Spine Society journal · 2023Article
- Identification of SMIM1 and SEZ6L2 as Potential Biomarkers for Genes Associated with Intervertebral Disc Degeneration in Pyroptosis.Disease markers · 2022Article
- Krüppel like factor 10 prevents intervertebral disc degeneration via TGF-β signaling pathway bothJournal of orthopaedic translation · 2021Article
- The c-Jun signaling pathway has a protective effect on nucleus pulposus cells in patients with intervertebral disc degeneration.Experimental and therapeutic medicine · 2020Article
- Sirt6 overexpression suppresses senescence and apoptosis of nucleus pulposus cells by inducing autophagy in a model of intervertebral disc degeneration.Cell death & disease · 2018Article
- Article
- Transforming growth factor β controls CCN3 expression in nucleus pulposus cells of the intervertebral disc.Arthritis and rheumatism · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAlthough transforming growth factor beta1 (TGFbeta1) is known to be a potent inhibitor of proliferation in most cell types, it accelerates proliferation in certain mesenchymal cells, such as articular chondrocytes and nucleus pulposus cells. The low ability for self-renewal of nucleus pulposus cells is one obstacle in developing new therapeutic options for intervertebral disc diseases, and utilizing cytokines is one of the strategies to regulate nucleus pulposus cell proliferation. However, the precise cell cycle progression and molecular mechanisms by which TGFbeta1 stimulates cell growth remain unclear. The aim of this study was to elucidate a mechanism that enables cell proliferation with TGFbeta1 stimulation.
methodsWe tested cultured rat nucleus pulposus cells for proliferation and cell cycle distribution under exogenous TGFbeta1 stimulation with and without putative pharmaceutical inhibitors. To understand the molecular mechanism, we evaluated the expression levels of key regulatory G1 phase proteins, c-Myc and the cyclin-dependent kinase inhibitors.
resultsWe found that TGFbeta1 promoted proliferation and cell cycle progression while reducing expression of the cyclin-dependent kinase inhibitors p21 and p27, which are downregulators of the cell cycle. Robust c-Myc expression for 2 h and immediate phosphorylation of extra cellular signal regulated kinase (ERK1/2) were detected in cultures when TGFbeta1 was added. However, pretreatment with 10058-F4 (an inhibitor of c-Myc transcriptional activity) or PD98059 (an inhibitor of ERK1/2) suppressed c-Myc expression and ERK1/2 phosphorylation, and inhibited cell cycle promotion by TGFbeta1.
conclusionsOur experimental results indicate that TGFbeta1 promotes cell proliferation and cell cycle progression in rat nucleus pulposus cells and that c-Myc and phosphorylated ERK1/2 play important roles in this mechanism. While the difference between rat and human disc tissues requires future studies using different species, investigation of distinct response in the rat model provides fundamental information to elucidate a specific regulatory pathway of TGFbeta1.
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