ArticleOsteoarthritis and cartilage2010
p38gamma mitogen-activated protein kinase suppresses chondrocyte production of MMP-13 in response to catabolic stimulation.
Article in Osteoarthritis and cartilage, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 33 citations in OpenAlex.
- Cellular Products with Anti-Inflammatory Properties for the Treatment of Cartilage Lesions.International journal of molecular sciences · 2026Review
- Potential Benefits of Glycine, Proline and Hydroxyproline on Growth and Flesh Quality of Mirror Carp (International journal of molecular sciences · 2025Article
- Post-translational modifications of collagen and its related diseases in metabolic pathways.Acta pharmaceutica Sinica. B · 2025Review
- Distinct effect of preconditioning with p38 MAPK signals on matrix-expanded human synovium-derived stem cell chondrogenesis: sb203580 favors chondrogenic differentiation while anisomycin benefits endochondral bone formation.Frontiers in cell and developmental biology · 2025Article
- Epigenetics and Herbs: Potential Therapeutic Strategies for Osteoarthritis of the Knee.Journal of pain research · 2025Review
- Hesperetin Attenuates T-2 Toxin-Induced Chondrocyte Injury by Inhibiting the p38 MAPK Signaling Pathway.Nutrients · 2024Article
- Targeting the senescence-related genes MAPK12 and FOS to alleviate osteoarthritis.Journal of orthopaedic translation · 2024Article
- G-quadruplex structural dynamics at MAPK12 promoter dictates transcriptional switch to determine stemness in breast cancer.Cellular and molecular life sciences : CMLS · 2024Article
- The role and mechanism of biological collagen membranes in repairing cartilage injury through the p38MAPK signaling pathway.Journal of orthopaedic surgery and research · 2023Article
- Isoform-specific optical activation of kinase function reveals p38-ERK signaling crosstalk.RSC chemical biology · 2023Article
- Review
- Rongjin Niantong Fang ameliorates cartilage degeneration by regulating the SDF-1/CXCR4-p38MAPK signalling pathway.Pharmaceutical biology · 2022Article
- Review
- TGF-β type 2 receptor-mediated modulation of the IL-36 family can be therapeutically targeted in osteoarthritis.Science translational medicine · 2019Article
- The effects of interleukin-1β in modulating osteoclast-conditioned medium's influence on gelatinases in chondrocytes through mitogen-activated protein kinases.International journal of oral science · 2015Article
- Nanocomposite scaffold for chondrocyte growth and cartilage tissue engineering: effects of carbon nanotube surface functionalization.Tissue engineering. Part A · 2014Article
- Pro-inflammatory stimulation of meniscus cells increases production of matrix metalloproteinases and additional catabolic factors involved in osteoarthritis pathogenesis.Osteoarthritis and cartilage · 2014Article
- Ionizing radiation causes active degradation and reduces matrix synthesis in articular cartilage.International journal of radiation biology · 2013Article
- Chondrogenesis, chondrocyte differentiation, and articular cartilage metabolism in health and osteoarthritis.Therapeutic advances in musculoskeletal disease · 2012Article
- New Insights into the p38γ and p38δ MAPK Pathways.Journal of signal transduction · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe signaling protein p38 mitogen-activated protein kinase is required for inflammatory signaling in chondrocytes that regulates matrix metalloproteinase (MMP) production. We sought to determine the role of specific p38 isoforms in chondrocyte catabolic signaling in response to IL-1beta and fibronectin fragments (Fn-f).
methodsHuman articular chondrocytes isolated from normal ankle cartilage from tissue donors or from osteoarthritic knee cartilage obtained during knee replacement were stimulated with IL-1beta or Fn-f, with or without pretreatment with p38 inhibitors (SB203580 or BIRB796) or growth factors (IGF-1 and OP-1). p38 isoform phosphorylation was measured by antibody array and immunoblotting. MMP-13 expression was measured by real-time polymerase chain reaction (PCR), enzyme-linked immunosorbent assay (ELISA), and immunoblotting. Chondrocytes were transfected with plasmids expressing constitutively active (CA) p38gamma or with adenovirus expressing dominant negative (DN) p38gamma.
resultsStimulation of chondrocytes with either IL-1beta or Fn-f led to enhanced phosphorylation of p38alpha and p38gamma, with little phosphorylation of p38beta or p38delta isoforms. p38alpha localized to the nucleus and p38gamma to the cytosol. Inhibition of both p38alpha and p38gamma with BIRB796 resulted in less inhibition of MMP-13 production in response to IL-1beta or FN-f than did inhibition of only p38alpha with SB203580. Transfection with CA p38gamma resulted in decreased MMP-13 production while transduction with DN p38gamma resulted in increased MMP-13 production. IGF-1 and OP-1 pretreatment inhibited p38alpha phosphorylation but not p38gamma phosphorylation.
conclusionsp38gamma is activated by catabolic stimulation of human articular chondrocytes, but interestingly suppresses MMP-13 production. Treatments that increase p38gamma activation may be of therapeutic benefit in reducing chondrocyte production of MMP-13.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.