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      Assessment of Cardiovascular Fibrosis Using Novel Fluorescent Probes

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          Abstract

          Cardiovascular fibrosis resulted from pressure overload or ischemia could alter myocardial stiffness and lead to ventricular dysfunction. Fluorescently labeled collagen-binding protein CNA 35, derived from the surface component of Staphylococcus aureus, and a novel synthetic biphenylalanine containing peptide are applied to stain fibrosis associated collagen and myocytes, respectively. Detailed pathological characteristics of cardiovascular fibrosis could be identified clearly in 2 hours. This staining pair requires only simple staining and brief washing, generating less than 10 ml of waste. The image information collected by this novel fluorescent staining pair is compatible with it collected by the traditional Masson's Trichrome and Picrosirius Red staining which are widely used to stain cardiovascular fibrosis and isolated cells.

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          Hormones and hemodynamics in heart failure.

          W Abraham, R Schrier (1999)
          Article 0 comments Cited 169 times – based on 0 reviews     Review now
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            Periostin induces proliferation of differentiated cardiomyocytes and promotes cardiac repair.

            Bernhard Kuhn, Federica del Monte, Roger J. Hajjar … (2007)
            Adult mammalian hearts respond to injury with scar formation and not with cardiomyocyte proliferation, the cellular basis of regeneration. Although cardiogenic progenitor cells may maintain myocardial turnover, they do not give rise to a robust regenerative response. Here we show that extracellular periostin induced reentry of differentiated mammalian cardiomyocytes into the cell cycle. Periostin stimulated mononucleated cardiomyocytes to go through the full mitotic cell cycle. Periostin activated alphaV, beta1, beta3 and beta5 integrins located in the cardiomyocyte cell membrane. Activation of phosphatidylinositol-3-OH kinase was required for periostin-induced reentry of cardiomyocytes into the cell cycle and was sufficient for cell-cycle reentry in the absence of periostin. After myocardial infarction, periostin-induced cardiomyocyte cell-cycle reentry and mitosis were associated with improved ventricular remodeling and myocardial function, reduced fibrosis and infarct size, and increased angiogenesis. Thus, periostin and the pathway that it regulates may provide a target for innovative strategies to treat heart failure.
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              From left ventricular hypertrophy to congestive heart failure: management of hypertensive heart disease.

              Alan Gradman, Fadi Alfayoumi (2015)
              Other than age, left ventricular hypertrophy (LVH) is the most potent predictor of adverse cardiovascular outcomes in the hypertensive population, and is an independent risk factor for coronary heart disease, sudden death, heart failure and stroke. Although directly related to systolic blood pressure, other factors including age, sex, race, body mass index and stimulation of the renin-angiotensin-aldosterone and sympathetic nervous systems play an important role in the pathogenesis of LVH. LVH involves changes in myocardial tissue architecture consisting of perivascular and myocardial fibrosis and medial thickening of intramyocardial coronary arteries, in addition to myocyte hypertrophy. The physiologic alterations which occur as a result of these anatomical changes include disturbances of myocardial blood flow, the development of an arrhythmogenic myocardial substrate and diastolic dysfunction. The latter is directly related to the degree of myocardial fibrosis and is the hemodynamic hallmark of hypertensive heart disease. When diastolic dysfunction is present, left ventricular end-diastolic pressure increases out-of-proportion to volume and may be elevated at rest or with exertion leading to clinical heart failure. At least one third of heart failure patients in the United States can be considered to have heart failure related to diastolic dysfunction. Compared to heart failure patients with systolic dysfunction, diastolic heart failure patients are more likely to be older, female, and to be hypertensive at the time of presentation. Although it has been assumed that LVH may lead to systolic dysfunction, evidence is lacking that LVH resulting from hypertension is a major risk factor for systolic heart failure independent of coronary artery disease. Treatment of hypertension greatly attenuates the development of LVH and significantly decreases the incidence of heart failure. In patients with established LVH, regression is both possible and desirable and results in a significant reduction in adverse clinical endpoints.
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                Author and article information

                Contributors
                : Role: Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, USA )
                ISSN (Electronic): 1932-6203
                Publication date Collection: 2011
                Publication date (Electronic): 20 April 2011
                Volume: 6
                Issue: 4
                Electronic Location Identifier: e19097
                Affiliations
                [1 ]Cardiovascular Research Center, Mount Sinai School of Medicine, New York, New York, United States of America
                [2 ]Department of Radiology, The Methodist Hospital Research Institute, Weill Medical College of Cornell University, Houston, Texas, United States of America
                Heart Center Munich, Germany
                Author notes

                Conceived and designed the experiments: JC SKL WRAE CHT. Performed the experiments: JC SKL WRAE LL EYG. Analyzed the data: JC SKL WRAE LL EYG RJH CHT. Contributed reagents/materials/analysis tools: JC SKL WRAE. Wrote the paper: JC SKL WRAE LL EYG RJH CHT.

                Article
                Publisher ID: PONE-D-11-00554
                DOI: 10.1371/journal.pone.0019097
                PMC ID: 3080412
                PubMed ID: 21533060
                SO-VID: c5146f57-5061-46dc-ae3b-7611ef55fe40
                Copyright © Chen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
                History
                Date received : 17 December 2010
                Date accepted : 16 March 2011
                Page count
                Pages: 6
                Categories
                Subject: Research Article
                Subject: Medicine
                Subject: Cardiovascular
                Subject: Acute Cardiovascular Problems
                Subject: Diagnostic Medicine
                Subject: Pathology
                Subject: Anatomical Pathology
                Subject: Histopathology
                Subject: General Pathology
                Subject: Molecular Pathology

                ScienceOpen disciplines: Uncategorized
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                ScienceOpen disciplines: Uncategorized

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