ArticleHistochemistry and cell biology2010
Extra cellular matrix remodelling after heterotopic rat heart transplantation: gene expression profiling and involvement of ED-A+ fibronectin, alpha-smooth muscle actin and B+ tenascin-C in chronic cardiac allograft rejection.
Article in Histochemistry and cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Longitudinal progression of tissue remodeling in experimental pulmonary hypertension is accompanied by a continuously increasing re-expression of extra domain A-containing fibronectin.Histochemistry and cell biology · 2026Article
- Review
- Serum Liberation of Fetal Fibronectin Variants in Patients with Pulmonary Hypertension: ED-AJournal of clinical medicine · 2021Article
- Danger signals in regulating the immune response to solid organ transplantation.The Journal of clinical investigation · 2017Review
- Article
- Detection of Soluble ED-A(+) Fibronectin and Evaluation as Novel Serum Biomarker for Cardiac Tissue Remodeling.Disease markers · 2016Article
- Comparative mRNA and MicroRNA Profiling during Acute Myocardial Infarction Induced by Coronary Occlusion and Ablation Radio-Frequency Currents.Frontiers in physiology · 2016Article
- Tenascin-C in cardiovascular remodeling: potential impact for diagnosis, prognosis estimation and targeted therapy.Cell adhesion & migration · 2015Review
- De novo expression of fetal ED-A(+) fibronectin and B (+) tenascin-C splicing variants in human cardiac allografts: potential impact for targeted therapy of rejection.Journal of molecular histology · 2014Article
- The pathogenesis of cardiac fibrosis.Cellular and molecular life sciences : CMLS · 2014Review
- Recipient-derived EDA fibronectin promotes cardiac allograft fibrosis.The Journal of pathology · 2012Article
- Advances in tenascin-C biology.Cellular and molecular life sciences : CMLS · 2011Review
- Histochemistry and cell biology: the annual review 2010.Histochemistry and cell biology · 2011Review
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic cardiac rejection is represented by cardiac allograft vasculopathy (CAV) and cardiac interstitial fibrosis (CIF) known to cause severe complications. These processes are accompanied by remarkable changes in the cardiac extra cellular matrix (cECM). The aim of our study was to analyse the cECM remodelling in chronic rejection and to elucidate a potential role of ED-A domain containing fibronectin (ED-A(+) Fn), alpha smooth muscle actin (ASMA) and B domain containing tenascin-C (B(+) Tn-C). A model of chronic rejection after heterotopic rat heart transplantation was used. Allografts, recipient and control hearts were subjected to histological assessment of rejection grade, to real-time PCR based analysis of 84 genes of ECM and adhesion molecules and to immunofluorescence labelling procedures, including ED-A(+) Fn, ASMA and B(+) Tn-C antibodies. Histological analysis revealed different grades of chronic rejection. By gene expression analysis, a relevant up-regulation of the majority of ECM genes in association with chronic rejection could be shown. For 8 genes, there was a relevant up-regulation in allografts as well as in the corresponding recipient hearts. Association of ASMA positive cells with the grade of chronic rejection could be proven. In CAV and also in CIF there were extensive co-depositions of ED-A(+) Fn, ASMA and B(+) Tn-C. In conclusion, chronic cardiac allograft rejection is associated with a cECM remodelling. ASMA protein deposition in CAV, and CIF is a valuable marker to detect chronic rejection. Interactions of VSMCs and Fibro-/Myofibroblasts with ED-A(+) Fn and B(+) Tn-C might functionally contribute to the development of chronic cardiac rejection.
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Registered trials
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