ArticlePloS one2014
Impact of ischemia-reperfusion on extracellular matrix processing and structure of the basement membrane of the heart.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 28 citations in OpenAlex.
- Single Cell Sequencing Reveals Mechanisms of Persistent Truncus Arteriosus Formation afterGenes · 2022Article
- Basement Membrane Extracellular Matrix Proteins in Pulmonary Vascular and Right Ventricular Remodeling in Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2021Article
- Article
- Extracellular Matrix in Ischemic Heart Disease, Part 4/4: JACC Focus Seminar.Journal of the American College of Cardiology · 2020Review
- The Non-Fibrillar Side of Fibrosis: Contribution of the Basement Membrane, Proteoglycans, and Glycoproteins to Myocardial Fibrosis.Journal of cardiovascular development and disease · 2019Review
- Cathepsin S degrades arresten and canstatin in infarcted area after myocardial infarction in rats.The Journal of veterinary medical science · 2019Article
- Transcatheter valve-in-valve implantation (VinV-TAVR) for failed surgical aortic bioprosthetic valves.Clinical research in cardiology : official journal of the German Cardiac Society · 2019Article
- Understanding cardiac extracellular matrix remodeling to develop biomarkers of myocardial infarction outcomes.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- T3 peptide, a fragment of tumstatin, stimulates proliferation and migration of cardiac fibroblasts through activation of Akt signaling pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2017Article
- The extracellular matrix in myocardial injury, repair, and remodeling.The Journal of clinical investigation · 2017Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeAcute ischemic injury is a strong inductor of cardiac remodelling, resulting in structural changes of the extracellular matrix (ECM) and basement membrane (BM). In a large animal model of ischemia-reperfusion (I/R) we investigated the post-ischemic liberation of the collagen-IV-fragments Tumstatin (TUM; 28 kDa-fragment of collagen-IV-alpha-3), Arresten (ARR; 26 kDa-fragment of collagen-IV-alpha-1) and Endorepellin (LG3, 85 kDa-fragment of perlecan) which are biologically active in angiogenesis and vascularization in the post-ischemic myocardium. METHODS AND
resultsIn this blinded study, 30 pigs were randomized to 60 min of global I/R at either 4°C or 32°C or served as control. Three transmyocardial tissue samples were collected prior to ischemia and within 30 min and 150 min of reperfusion. Tissue content of TUM, ARR and LG3 was analyzed by western blotting and immunostaining. Within 150 min of mild hypothermic I/R a significantly increased tissue content of ARR (0.17±0.14 vs. 0.56±0.56; p = 0.001) and LG3 (1.13±0.34 vs. 2.51±1.71, p<0.001) was observed. In contrast, deep hypothermic I/R was not associated with a significant release of cleavage products. Cleavage of TUM remained unchanged irrespective of temperature. Increased matrix processing following mild hypothermia I/R is further supported by a >11fold elevation of creatine kinase (2075±2595 U/l vs. 23248±6551 U/l; p<0.001) in the coronary sinus plasma samples. Immunostaining demonstrated no changes for ARR and LG3 presentation irrespective of temperature. In contrast, TUM significantly decreased in the BM surrounding cardiomyocytes and capillaries after mild and deep hypothermic I/R, thus representing structural alterations of the BM in these groups.
conclusionThe study demonstrates an early temperature-dependent processing of Col-IV as major component of the BM of cardiomyocytes and vascular endothelium. These observations support the protective effects of deep hypothermia during I/R. Furthermore, the results suggest an increased structural remodelling of the myocardial basement membrane with potential functional impairment during mild hypothermic I/R which may contribute to the progression to post-ischemic heart failure.
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