ArticleClinical and experimental immunology2009
Synergistic effects of cyclic strain and Th1-like cytokines on tenascin-C production by rheumatic aortic valve interstitial cells.
Article in Clinical and experimental immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.
- Systemic Soluble and Cellular Immune Response in Acute Rheumatic Fever and Rheumatic Heart Disease: A Systematic Review of Human Studies.Pathogens (Basel, Switzerland) · 2025Pooled it
- Methods for Establishing a Rat Model of Rheumatic Heart Disease.Reviews in cardiovascular medicine · 2024Review
- IgG2 rules: N-acetyl-β-D-glucosamine-specific IgG2 and Th17/Th1 cooperation may promote the pathogenesis of acute rheumatic heart disease and be a biomarker of the autoimmune sequelae ofFrontiers in cardiovascular medicine · 2022Article
- Interference with the expression of S1PR1 or STAT3 attenuates valvular damage due to rheumatic heart disease.International journal of molecular medicine · 2021Article
- Signalling pathways implicated in the pathogenesis of rheumatic heart disease (Review).Experimental and therapeutic medicine · 2021Review
- Article
- Revisiting the matricellular concept.Matrix biology : journal of the International Society for Matrix Biology · 2014Review
- Polymethoxy flavones do not exert an inducing effect on the biosynthesis and secretion of insulin by pancreatic β-cells.Biomedical reports · 2014Article
- mTOR signal transduction pathways contribute to TN-C FNIII A1 overexpression by mechanical stress in osteosarcoma cells.Molecules and cells · 2014Article
- An investigation of tenascin-C levels in rheumatic mitral stenosis and their response to percutaneous mitral balloon valvuloplasty.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2013Article
- Tenascin-C produced by oxidized LDL-stimulated macrophages increases foam cell formation through Toll-like receptor-4.Molecules and cells · 2012Article
- Advances in tenascin-C biology.Cellular and molecular life sciences : CMLS · 2011Review
- Attenuated expression of tenascin-C in ovalbumin-challenged STAT4-/- mice.Respiratory research · 2011Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tenascin-C (TN-C) is a key component of extracellular matrix (ECM) and its expression process is poorly understood during rheumatic heart valvular disease (RHVD). In this study, we found that interferon (IFN)-gamma, tumour necrosis factor (TNF)-alpha and TN-C concentrations in patients with RHVD were significantly higher than in normal controls. More IFN-gamma receptors and TNF receptors were found being expressed on rheumatic aortic valves interstitial cells than on non-rheumatic ones and their expression was patients' sera dependent. Antibodies neutralizing IFN-gamma or TNF-alpha could attenuate patients' sera-induced TN-C transcription by isolated rheumatic aortic valves interstitial cells. By application with different protein kinase inhibitors, we found that combined with cyclic strain, TNF-alpha and IFN-gamma induced TN-C transcription through the RhoA/ROCK signalling pathway. At the same time, p38 mitogen-activated protein kinase was involved in TNF-alpha and IFN-gamma induced TN-C transcription. TNF-alpha also increased TN-C mRNA level by additional PKC and ERK 1/2 activation. Our finding revealed a new insight into ECM remodelling during RHVD pathogenesis and new mechanisms involved in the clinical anti-IFN-gamma and anti-TNF-alpha therapy.
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Registered trials
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