The impact of age on cardiac function and extracellular matrix component expression in adverse post-infarction remodeling in mice

Nagel, Felix; Santer, David; Stojković, Stefan; Kaun, Christoph; Schaefer, Anne‐Kristin; Krššák, Martin; Abraham, Dietmar; Bencsik, Péter; Ferdinándy, Péter; Kenyeres, Éva; Szabados, Tamara; Wojta, Johann; Trescher, Karola; Kiss, Attila; Podesser, Bruno K.

doi:10.1016/j.exger.2019.02.008

Cited by 7 publications

(4 citation statements)

References 55 publications

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“…4 Notably, in transmural MI, TN-C is up-regulated in the border zone, while it is expressed throughout the tissue in non-transmural MIs. Four weeks after MI, TN-C disappears from the scar, while TN-C expression sustains hibernating myocardium, 3,5 which underlines its role in cardiac remodelling. Conversely, TN-C knockout (KO) mice subjected to transverse aortic constriction showed a significant reduction in LV remodelling when compared with wild-type (WT) mice.…”

Section: Introductionmentioning

confidence: 93%

Tenascin‐C aggravates ventricular dilatation and angiotensin‐converting enzyme activity after myocardial infarction in mice

et al. 2020

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Aims Tenascin-C (TN-C) is suggested to be detrimental in cardiac remodelling after myocardial infarction (MI). The aim of this study is to reveal the effects of TN-C on extracellular matrix organization and its haemodynamic influence in an experimental mouse model of MI and in myocardial cell culture during hypoxic conditions. Methods and results Myocardial infarction was induced in TN-C knockout (TN-C KO) and wild-type mice. Six weeks later, cardiac function was studied by magnetic resonance imaging and under isolated working heart conditions. Myocardial mRNA levels and immunoreactivity of TN-C, TIMP-1, TIMP-3, and matrix metalloproteinase (MMP)-9, as well as serum and tissue activities of angiotensin-converting enzyme (ACE), were determined at 1 and 6 weeks after infarction. Cardiac output and external heart work were higher, while left ventricular wall stress and collagen expression were decreased (P < 0.05) in TN-C KO mice as compared with age-matched controls at 6 weeks after infarction. TIMP-1 expression was down-regulated at 1 and 6 weeks, and TIMP-3 expression was up-regulated at 1 week (P < 0.01) after infarction in knockout mice. MMP-9 level was lower in TN-C KO at 6 weeks after infarction (P < 0.05). TIMP-3/MMP-9 ratio was higher in knockout mice at 1 and 6 weeks after infarction (P < 0.01). ACE activity in the myocardial border zone (i.e. between scar and free wall) was significantly lower in knockout than in wild-type mice 1 week after MI (P < 0.05). Conclusions Tenascin-C expression is induced by hypoxia in association with ACE activity and MMP-2 and MMP-9 elevations, thereby promoting left ventricular dilatation after MI.

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Section: Introductionmentioning

confidence: 93%

Tenascin‐C aggravates ventricular dilatation and angiotensin‐converting enzyme activity after myocardial infarction in mice

et al. 2020

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“…The expression of TNC becomes detectable within 24 h of the onset of infarction in experimental animal models, peaks on days 3–5, and disappears by day 28 [ 25 , 54 , 58 ]. Serum levels of TNC in human patients reflect this time course of expression [ 59 ].…”

Section: Myocardial Infarctionmentioning

confidence: 99%

Tenascin-C in Heart Diseases—The Role of Inflammation

Imanaka‐Yoshida

2021

IJMS

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Tenascin-C (TNC) is a large extracellular matrix (ECM) glycoprotein and an original member of the matricellular protein family. TNC is transiently expressed in the heart during embryonic development, but is rarely detected in normal adults; however, its expression is strongly up-regulated with inflammation. Although neither TNC-knockout nor -overexpressing mice show a distinct phenotype, disease models using genetically engineered mice combined with in vitro experiments have revealed multiple significant roles for TNC in responses to injury and myocardial repair, particularly in the regulation of inflammation. In most cases, TNC appears to deteriorate adverse ventricular remodeling by aggravating inflammation/fibrosis. Furthermore, accumulating clinical evidence has shown that high TNC levels predict adverse ventricular remodeling and a poor prognosis in patients with various heart diseases. Since the importance of inflammation has attracted attention in the pathophysiology of heart diseases, this review will focus on the roles of TNC in various types of inflammatory reactions, such as myocardial infarction, hypertensive fibrosis, myocarditis caused by viral infection or autoimmunity, and dilated cardiomyopathy. The utility of TNC as a biomarker for the stratification of myocardial disease conditions and the selection of appropriate therapies will also be discussed from a clinical viewpoint.

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“…TNC и постинфарктное моделирование В патогенезе повреждения миокарда и сердечной дисфункции эксперименты на животных показали, что TNC участвует в ремоделировании миокарда при ИМ и миокардите. Также было отмечено, что TNC способствует усугублению гипертрофии миокарда, фиброзу и сердечной дисфункции у животных с гипертрофированным сердцем [15,[19][20][21][22][23][24][25].…”

Section: биологические аспекты Tncunclassified

“…Экспрессия матричной рибонуклеиновой кислоты MMP-2 (7d: p<0,05), TIMP-1 (7d: p<0,05), TIMP-2 (7d: p<0,05), коллагена-1 (3d и 7d: p<0,05) и коллагена-3 (7d: p<0,05) в здоровом миокарде ЛЖ была значительно выше у YM, чем у OM после ИМ. Активность ММП-9 в плазме у ОМ увеличивалась (3d: p<0,01), уровни TNC в плазме снизились у OM по сравнению с YM после развития ИМ (3d: p<0,001, 7d: p<0,05) [21].…”

Section: биологические аспекты Tncunclassified

Tenascin-C as a cardiovascular marker

et al. 2022

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Novel biological markers, such as fibrosis marker galectin-3, peptide hormone adrenomedullin, soluble ST2, chemokine CX3CL1, surrogate marker of vasopressin, and others, are every year one step closer to being introduced into health practice. Over the past decades, significant progress has been made in the study of cardiovascular biomarkers. A key moment was the introduction of deter mining the concentration of natriuretic peptides used as markers for the diagnostic and prognostic evaluation of patients with heart failure. Currently, in order to search for novel markers for early diagnosis and risk stratification, studies have been conducted on the analysis of promising inflammatory marker tenascin-C (TNC) in cardiovascular patients. Data have been obtained that allow us to consider TNC as a tool for risk stratification and assessment of cardiovascular disease prognosis. The combination of TNC with other biological markers, in particular brain natriuretic peptide, may improve prognostic power. Nevertheless, serial testing to assess the prognosis and effectiveness of ongoing treatment, including in the conditions of a multimarker model, requires further research.

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The impact of age on cardiac function and extracellular matrix component expression in adverse post-infarction remodeling in mice

Cited by 7 publications

References 55 publications

Tenascin‐C aggravates ventricular dilatation and angiotensin‐converting enzyme activity after myocardial infarction in mice

Tenascin‐C aggravates ventricular dilatation and angiotensin‐converting enzyme activity after myocardial infarction in mice

Tenascin-C in Heart Diseases—The Role of Inflammation

Tenascin-C as a cardiovascular marker

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