ArticleJournal of cellular and molecular medicine2017
Crosstalk between Smad2/3 and specific isoforms of ERK in TGF-β1-induced TIMP-3 expression in rat chondrocytes.
Article in Journal of cellular and molecular medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 29 citations in OpenAlex.
- Nucleus pulposus cell network modelling in the intervertebral disc.NPJ systems biology and applications · 2025Article
- Targeting PYK2, entrectinib allays anterior subcapsular cataracts in mice by regulating TGFβ2 signaling pathway.Molecular medicine (Cambridge, Mass.) · 2024Article
- Osteoarthritis: pathogenic signaling pathways and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Natural compounds protect against the pathogenesis of osteoarthritis by mediating the NRF2/ARE signaling.Frontiers in pharmacology · 2023Review
- The role of TGF-β2 in cartilage development and diseases.Bone & joint research · 2021Article
- IGF-1 protects against angiotensin II-induced cardiac fibrosis by targeting αSMA.Cell death & disease · 2021Article
- Crosstalk between the activated Slit2-Robo1 pathway and TGF-β1 signalling promotes cardiac fibrosis.ESC heart failure · 2021Article
- In the presence of TGF-β1, Asperosaponin VI promotes human mesenchymal stem cell differentiation into nucleus pulposus like- cells.BMC complementary medicine and therapies · 2021Article
- TIMP3/TGF‑β1 axis regulates mechanical loading‑induced chondrocyte degeneration and angiogenesis.Molecular medicine reports · 2020Article
- NMDA receptor-mediated CaMKII/ERK activation contributes to renal fibrosis.BMC nephrology · 2020Article
- TGFβ1-Smad canonical and -Erk noncanonical pathways participate in interleukin-17-induced epithelial-mesenchymal transition in Sjögren's syndrome.Laboratory investigation; a journal of technical methods and pathology · 2020Article
- Extracellular Signal-Regulated Kinase: A Regulator of Cell Growth, Inflammation, Chondrocyte and Bone Cell Receptor-Mediated Gene Expression.International journal of molecular sciences · 2019Review
- AMD3100 Attenuates Post-Traumatic Osteoarthritis by Maintaining Transforming Growth Factor-β1-Induced Expression of Tissue Inhibitor of Metalloproteinase-3Frontiers in pharmacology · 2019Article
- MEK inhibition prevents TGF‑β1‑induced myofibroblast transdifferentiation in human tenon fibroblasts.Molecular medicine reports · 2019Article
- Complement Activation During Ischemia/Reperfusion Injury Induces Pericyte-to-Myofibroblast Transdifferentiation Regulating Peritubular Capillary Lumen Reduction Through pERK Signaling.Frontiers in immunology · 2018Article
- [Effect of superparamagnetic iron oxide on differentiation of rat bone marrow stem cells into chondrocytes in vitro].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study investigated the roles of ERK1 and ERK2 in transforming growth factor-β1 (TGF-β1)-induced tissue inhibitor of metalloproteinases-3 (TIMP-3) expression in rat chondrocytes, and the specific roles of ERK1 and ERK2 in crosstalk with Smad2/3 were investigated to demonstrate the molecular mechanism of ERK1/2 regulation of TGF-β1 signalling. To examine the interaction of specific isoforms of ERK and the Smad2/3 signalling pathway, chondrocytes were infected with LV expressing either ERK1 or ERK2 siRNA and stimulated with or without TGF-β1. At indicated time-points, TIMP-3 expression was determined by real-time PCR and Western blotting; p-Smad3, nuclear p-Smad3, Smad2/3, p-ERK1/2 and ERK1/2 levels were assessed. And then, aggrecan, type II collagen and the intensity of matrix were examined. TGF-β1-induced TIMP-3 expression was significantly inhibited by ERK1 knock-down, and the decrease in TIMP-3 expression was accompanied by a reduction of p-Smad3 in ERK1 knock-down cells. Knock-down of ERK2 had no effect on neither TGF-β1-induced TIMP-3 expression nor the quantity of p-Smad3. Moreover, aggrecan, type II collagen expression and the intensity of matrix were significantly suppressed by ERK1 knock-down instead of ERK2 knock-down. Taken together, ERK1 and ERK2 have different roles in TGF-β1-induced TIMP-3 expression in rat chondrocytes. ERK1 instead of ERK2 can regulate TGF-β/Smad signalling, which may be the mechanism through which ERK1 regulates TGF-β1-induced TIMP-3 expression.
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