Post-transcriptional Regulation of Extracellular Matrix Metalloproteinase in Human Heart End-stage Failure Secondary to Ischemic Cardiomyopathy

Tyagi, Suresh C.; Kumar, Suresh; Haas, Steven Joseph; Reddy, Hanumanth K.; Voelker, Donald J.; Hayden, Melvin R.; Demmy, Todd L.; Schmaltz, Richard A.; Curtis, Jennifer

doi:10.1006/jmcc.1996.0132

Cited by 134 publications

(97 citation statements)

References 35 publications

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“…There has been considerable interest in the mechanism and extent of activation of the local MMP proteolytic system in human ischemic myocardium (7,8). Using ELISA, Spinale et al (4) found MMP-9 levels significantly increased and MMP-1 decreased markedly in tissue from explanted hearts in end-stage ICM patients.…”

Section: Discussionmentioning

confidence: 99%

“…La spironolactone peut supprimer partiellement la dysrégulation du métabolisme du collagène. the altered profile of the end products of collagen metabolism remain less well established (3,4,(6)(7)(8).…”

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“…Recent investigations indicate that CHF produces a relatively specific change in the spectrum of biomarkers of collagen metabolism and collagen types (7)(8)(9)(10). However, MMP species are not uniformly upregulated in heart failure; rather, this is dependent on different heart failure etiologies and different stimuli.…”

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confidence: 99%

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Treatment with spironolactone for 24 weeks decreases the level of matrix metalloproteinases and improves cardiac function in patients with chronic heart failure of ischemic etiology

Huang

Okello

et al. 2009

Canadian Journal of Cardiology

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Section: Discussionmentioning

confidence: 99%

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Treatment with spironolactone for 24 weeks decreases the level of matrix metalloproteinases and improves cardiac function in patients with chronic heart failure of ischemic etiology

Huang

Okello

et al. 2009

Canadian Journal of Cardiology

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“…ECM accumulation leads to increased endothelial to myocyte distance (20), and, recently, our laboratory showed that activation of MMPs leads to endothelialmyocyte uncoupling (21). There are Ͼ20 MMPs in the family, but MMP-2 and MMP-9 are the most robustly increased during the early and late phase of CHF, respectively (28).…”

mentioning

confidence: 98%

Role of matrix metalloproteinase-9 in endothelial apoptosis in chronic heart failure in mice

Ovechkin¹,

Tyagi²,

Rodríguez³

et al. 2005

Journal of Applied Physiology

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. Role of matrix metalloproteinase-9 in endothelial apoptosis in chronic heart failure in mice. J Appl Physiol 99: [2398][2399][2400][2401][2402][2403][2404][2405] 2005. First published August 4, 2005; doi:10.1152/japplphysiol.00442.2005.-Accumulation of oxidized extracellular matrix between endothelium and muscle is an important risk factor in the endothelium-myocytes uncoupling in congestive heart failure. Although ventricular remodeling is accompanied by increased matrix metalloproteinase (MMP)-9 activity, it is unclear whether MMP-9 plays a role in endothelial apoptosis in chronic volume overload congestive heart failure. We tested the hypothesis that, in chronic volume overload, myocardial dysfunction involves endocardial endothelial (EE) apoptosis in response to MMP-9 activation, extracellular matrix accumulation, and endotheliummyocytes uncoupling. Arteriovenous fistula (AVF) was created in control (FVB/NJ) and MMP-9 knockout (MMP-9KO; FVB.Cg-MMP9 tm1Tvu /J) mice. Sham surgery was used as control. Mice were grouped as follows: wild type, n ϭ 3 (sham control); MMP-9KO, n ϭ 3 (sham); AVF, n ϭ 3; and MMP-9KO ϩ AVF (n ϭ 3). Heart function was analyzed by M-mode and Doppler echocardiography, and with a pressure-tipped Millar catheter placed in the left ventricle of anesthetized mice 8 wk after AVF. Apoptosis was detected by measuring caspase-3, transferase-mediated dUTP nick-end labeling (TUNEL), and CD-31 by immunolabeling. Protease-activated receptors-1, connexin-43, and a disintegrin and MMP-12 (ADAM-12) expression were measured by Western blot analyses. MMP-2 and MMP-9 expression were measured by quantitative RT-PCR. Compared with control, AVF caused an increase in left ventricle end diastolic pressure and decrease in ϪdP/dt. In contrast, in the MMP-9KO ϩ AVF group, these variables were changed toward control levels. Increased EE apoptosis (caspase-3 activation and TUNEL/ CD-31 colabeling) in AVF mice was prevented in the MMP-9KO ϩ AVF group. Protease-activated receptor-1, connexin-43, and ADAM-12 were induced in AVF. MMP-9 gene ablation ameliorated the induction. The results suggest that impaired cardiac function in volume overload is associated with EE apoptosis, cardiac remodeling, and endothelium-myocytes uncoupling in response to MMP-9 activation. arteriovenous fistula; endocardial dysfunction; extracellular matrix remodeling; terminal deoxynucleotidyl nick-end labeling; connexin-43; protease-activated receptors-1; a disintegrin and metalloproteinase-12; congestive heart failure MYOCARDIAL REMODELING IN congestive heart failure (CHF) is associated with accumulation of extracellular matrix (ECM) between endothelial and muscle cells (21) and is one of the most important factors of endocardial endothelial dysfunction (8,14). Previous studies showed that morphological changes in myocardium are associated with increased expression and activity of matrix metalloproteinases (MMPs) (6, 18). MMPs degrade interstitial collagen and elastin, but the more collagen is degraded, the more that is synthesized. Consequ...

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“…Au nombre de quatre (TIMP-1 à -4), seule la TIMP-4 est plus ou moins spécifique du coeur [18]. Les données concernant l'expression des TIMP dans le postinfarctus sont disparates: on observe généralement des augmentations de l'expression de leurs ARNm [19][20][21][22], mais les résultats divergent au niveau protéique [23][24][25][26]. Cependant, une baisse des taux protéiques des TIMP est le plus souvent rapportée, qui reflète une régu-lation post-transcriptionnelle importante.…”

Section: Remodelage De La Matrice Extracellulaireunclassified

Remodelage précoce du ventricule gauche après un accident coronarien aigu

et al. 2004

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Post-transcriptional Regulation of Extracellular Matrix Metalloproteinase in Human Heart End-stage Failure Secondary to Ischemic Cardiomyopathy

Cited by 134 publications

References 35 publications

Treatment with spironolactone for 24 weeks decreases the level of matrix metalloproteinases and improves cardiac function in patients with chronic heart failure of ischemic etiology

Treatment with spironolactone for 24 weeks decreases the level of matrix metalloproteinases and improves cardiac function in patients with chronic heart failure of ischemic etiology

Role of matrix metalloproteinase-9 in endothelial apoptosis in chronic heart failure in mice

Remodelage précoce du ventricule gauche après un accident coronarien aigu

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