ArticleArthritis research & therapy2005
Tumor necrosis factor alpha and epidermal growth factor act additively to inhibit matrix gene expression by chondrocyte.
Article in Arthritis research & therapy, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- Meta-analysis of tumor necrosis factor alpha -308 polymorphism and knee osteoarthritis risk.BMC musculoskeletal disorders · 2014Pooled it
- Platelet-Rich Plasma for Degenerative Spine Disease: A Brief Overview.Spine surgery and related research · 2024Review
- Investigation of the efficacy of epidermal growth factor, boric acid and their combination in cartilage injury in rats: An experimental study.Joint diseases and related surgery · 2024Article
- Effects and action mechanisms of individual cytokines contained in PRP on osteoarthritis.Journal of orthopaedic surgery and research · 2023Review
- Inhibition of the extracellular signal-regulated kinase pathway reduces the inflammatory component in nucleus pulposus cells.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2022Article
- Therapeutic Potential of Dental Pulp Stem Cells and Leukocyte- and Platelet-Rich Fibrin for Osteoarthritis.Cells · 2020Article
- The TGFα-EGFR-Akt signaling axis plays a role in enhancing proinflammatory chemokines in triple-negative breast cancer cells.Oncotarget · 2018Article
- Protective effects of C-type natriuretic peptide on linear growth and articular cartilage integrity in a mouse model of inflammatory arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2014Article
- Characteristics of chemokine signatures elicited by EGF and TNF in ovarian cancer cells.Journal of inflammation (London, England) · 2013Article
- Transient anabolic effects accompany epidermal growth factor receptor signal activation in articular cartilage in vivo.Arthritis research & therapy · 2013Article
- Nicotinamide phosphoribosyltransferase is essential for interleukin-1beta-mediated dedifferentiation of articular chondrocytes via SIRT1 and extracellular signal-regulated kinase (ERK) complex signaling.The Journal of biological chemistry · 2011Article
- Article
- Protein biochip array technology to monitor rituximab in rheumatoid arthritis.Clinical and experimental immunology · 2009Article
- Egr-1 inhibits the expression of extracellular matrix genes in chondrocytes by TNFalpha-induced MEK/ERK signalling.Arthritis research & therapy · 2009Article
- Protein biochip array technology for cytokine profiling predicts etanercept responsiveness in rheumatoid arthritis.Clinical and experimental immunology · 2008Article
- Regulation of Sox9 activity by crosstalk with nuclear factor-kappaB and retinoic acid receptors.Arthritis research & therapy · 2008Article
- Prostaglandin E2 receptors EP1 and EP4 are up-regulated in rabbit chondrocytes by IL-1beta, but not by TNFalpha.Rheumatology international · 2007Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The failure of chondrocytes to replace the lost extracellular matrix contributes to the progression of degenerative disorders of cartilage. Inflammatory mediators present in the joint regulate the breakdown of the established matrix and the synthesis of new extracellular matrix molecules. In the present study, we investigated the effects of tumor necrosis factor alpha (TNF-alpha) and epidermal growth factor (EGF) on chondrocyte morphology and matrix gene expression. Chondrocytes were isolated from distal femoral condyles of neonatal rats. Cells in primary culture displayed a cobblestone appearance. EGF, but not TNF-alpha, increased the number of cells exhibiting an elongated morphology. TNF-alpha potentiated the effect of EGF on chondrocyte morphology. Individually, TNF-alpha and EGF diminished levels of aggrecan and type II collagen mRNA. In combination, the effects of TNF-alpha and EGF were additive, indicating the involvement of discrete signaling pathways. Cell viability was not compromised by TNF-alpha or by EGF, alone or in combination. EGF alone did not activate NF-kappaB or alter NF-kappaB activation by TNF-alpha. Pharmacologic studies indicated that the effects of TNF-alpha and EGF alone or in combination were independent of protein kinase C signaling, but were dependent on MEK1/2 activity. Finally, we analyzed the involvement of Sox-9 using a reporter construct of the 48 base pair minimal enhancer of type II collagen. TNF-alpha attenuated enhancer activity as expected; in contrast, EGF did not alter either the effect of TNF-alpha or basal activity. TNF-alpha and EGF, acting through distinct signaling pathways, thus have additive adverse effects on chondrocyte function. These findings provide critical insights into the control of chondrocytes through the integration of multiple extracellular signals.
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