Matrix metalloproteinase expression in cardiac myocytes following myocardial infarction in the rabbit

Romanic, Anne M.; Burns-Kurtis, Cynthia L.; Gout, Bernard; Berrebi-Bertrand, Isabelle; Ohlstein, Eliot H.

doi:10.1016/s0024-3205(00)00982-6

Cited by 116 publications

(85 citation statements)

References 22 publications

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“…1B and 2A) might be mainly due to the infiltrated neutrophils. Although all cell types, including cardiomyocytes (25,34) and endothelial cells (41), express MMP-9, neutrophil is an important source of MMP-9 after I/R (26). The level of endogenous active MMP-9 was lower in the I/R-VS group than in the I/R group (Fig.…”

Section: Discussionmentioning

confidence: 90%

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Efferent vagal nerve stimulation induces tissue inhibitor of metalloproteinase-1 in myocardial ischemia-reperfusion injury in rabbit

Uemura

Tsutsumi

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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August 10, 2007; doi:10.1152/ajpheart.00490.2007.-Vagal nerve stimulation has been suggested to ameliorate left ventricular (LV) remodeling in heart failure. However, it is not known whether and to what degree vagal nerve stimulation affects matrix metalloproteinase (MMP) and tissue inhibitor of MMP (TIMP) in myocardium, which are known to play crucial roles in LV remodeling. We therefore investigated the effects of electrical stimulation of efferent vagal nerve on myocardial expression and activation of MMPs and TIMPs in a rabbit model of myocardial ischemia-reperfusion (I/R) injury. Anesthetized rabbits were subjected to 60 min of left coronary artery occlusion and 180 min of reperfusion with (I/R-VS, n ϭ 8) or without vagal nerve stimulation (I/R, n ϭ 7). Rabbits not subjected to coronary occlusion with (VS, n ϭ 7) or without vagal stimulation (sham, n ϭ 7) were used as controls. Total MMP-9 protein increased significantly after left coronary artery occlusion in I/R-VS and I/R to a similar degree compared with VS and sham values. Endogenous active MMP-9 protein level was significantly lower in I/R-VS compared with I/R. TIMP-1 mRNA expression was significantly increased in I/R-VS compared with the I/R, VS, and sham groups. TIMP-1 protein was significantly increased in I/R-VS and VS compared with the I/R and sham groups. Cardiac microdialysis technique demonstrated that topical perfusion of acetylcholine increased dialysate TIMP-1 protein level, which was suppressed by coperfusion of atropine. Immunohistochemistry demonstrated a strong expression of TIMP-1 protein in cardiomyocytes around the dialysis probe used to perfuse acetylcholine. In conclusion, in a rabbit model of myocardial I/R injury, vagal nerve stimulation induced TIMP-1 expression in cardiomyocytes and reduced active MMP-9. myocardial remodeling; matrix metalloproteinase; acetylcholine LEFT VENTRICULAR (LV) myocardial remodeling that occurs after myocardial infarction (MI) leads to progressive LV dilation and eventually pump dysfunction (33,40). In addition to the loss of contractile cardiomyocytes, pathological degradation and reconstitution of extracellular matrix significantly contribute to the progression of LV remodeling, where matrix metalloproteinase (MMP) and its intrinsic inhibitor, tissue inhibitor of MMP (TIMP), play crucial roles (37,43).A previous study using genetically engineered mice demonstrated that target deletion of the MMP-9 gene prevented LV rupture and ameliorated LV remodeling after MI (10). The positive results of MMP inhibition on LV remodeling in animal models led to the proposal to use MMP inhibitors as a potential therapy for patients at risk for the development of heart failure after MI (27, 32). However, recent clinical results from the Prevention of Myocardial Infarction Early Remodeling (PREMIER) trial failed to demonstrate a beneficial effect of MMP inhibition on LV remodeling after MI (16). This indicates the importance of further understanding the in vivo regulatory mechanisms of MMPs to understand and benefic...

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Section: Discussionmentioning

confidence: 90%

“…In addition to cardiomyocytes (25,34), a variety of cell types, such as fibroblasts (14) and endothelial cells (6), produces and secretes TIMP-1. TIMP-1 expression in these cell types is low in the basal condition but is transcriptionally induced by various agents, including the cytokines, serum, growth factors, and phorbol esters (14).…”

Section: Discussionmentioning

confidence: 99%

Efferent vagal nerve stimulation induces tissue inhibitor of metalloproteinase-1 in myocardial ischemia-reperfusion injury in rabbit

Uemura

Tsutsumi

et al. 2007

American Journal of Physiology-Heart and Circulatory Physiology

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“…A study of acute post-MI induction of MMPs in rabbit showed a similar pattern of elevated MMP-2, 3, and -9, without evidence of increased MMP-13. [19] This complement of MMPs induced by IL-1β, combined with the absence of MMP-13 (rodent native fibrillar collagenase), suggests that IL-1β directs metabolism of degraded fibrillar collagens, native collagen III, or non-collagenous ECM such as basement membrane, rather than indiscriminate degradation of structurally sound fibrillar collagen I, the majority ECM constituent. [20] Further, IL-1β strongly increased TIMP-1, supporting the interpretation of selective and tightly controlled ECM metabolism.…”

Section: Discussionmentioning

confidence: 99%

Cytokines regulate matrix metalloproteinases and migration in cardiac fibroblasts

Brown

Jones

Laird

et al. 2007

Biochemical and Biophysical Research Communications

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We sought to define the relationship between cytokine stimulated release of matrix metalloproteinases (MMPs) and cell migration using adult rat cardiac fibroblasts. Interleukin-1β (IL-1β) increased release of MMP-2, 3, and 9, and TIMP-1, by 3-6-fold, measured by immunoblotting and gel zymography. Tumor necrosis factor-α (TNFα) augmented IL-1 stimulated release of MMP-9, but not MMP-2 or -3. Transforming growth factor-β1 (TGFβ1) attenuated all the responses to IL-1β. IL-1β was also the most robust stimulus of adult rat cardiac fibroblast migration, measured in Boyden chamber assays. The combination of IL-1β plus TNFα substantially enhanced migration, whereas TGFβ1 strongly inhibited the migratory response to IL-1β. The pan-selective MMP inhibitor GM 6001 effectively blocked IL-1β stimulated migration. Pharmacologic inhibitors selective for ERK, JNK, and p38 MAP kinase pathways inhibited the IL-1β regulation of individual MMPs. Increased MMP activity associated with migration of cardiac fibroblasts may be important determinants of cytokine-directed remodeling of injured myocardium.

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“…3,4 A reduction in myocardial TIMP-1, in particular, is significantly associated with ischemic heart failure in human patients 5 and in animal models. 6 An imbalance between TIMP and MMP expression appears to be responsible for the increased MMP activity observed in congestive heart failure, which is associated with myocardial matrix collagen disruption and ventricular remodeling. 4,7,8 Disruption of the ECM impairs myocardial contractile function and promotes ventricular dilation and wall thinning.…”

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confidence: 99%

Inhibition of Matrix Metalloproteinase Activity by TIMP-1 Gene Transfer Effectively Treats Ischemic Cardiomyopathy

et al. 2004

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Background-Enhanced activity of matrix metalloproteinases (MMPs) has been associated with extracellular matrix degradation and ischemic heart failure in animal models and human patients. This study evaluated the effects of MMP inhibition by gene transfer of TIMP-1 in a rat model of ischemic cardiomyopathy. Methods and Results-Rats underwent ligation of the left anterior descending coronary artery with direct intramyocardial injection of replication-deficient adenovirus encoding TIMP-1 (nϭ8) or null virus as control vector (nϭ8), and animals were analyzed after 6 weeks. Both systolic and diastolic cardiac function was significantly preserved in the TIMP-1 group compared with control animals (maximum left ventricular [LV] pressure: TIMP-1 70Ϯ10 versus control 56Ϯ12 mmHg, PϽ0.05; maximum dP/dt 2697Ϯ842 versus 1622Ϯ527 mmHg/sec, PϽ0.01; minimum dP/dt

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Matrix metalloproteinase expression in cardiac myocytes following myocardial infarction in the rabbit

Cited by 116 publications

References 22 publications

Efferent vagal nerve stimulation induces tissue inhibitor of metalloproteinase-1 in myocardial ischemia-reperfusion injury in rabbit

Efferent vagal nerve stimulation induces tissue inhibitor of metalloproteinase-1 in myocardial ischemia-reperfusion injury in rabbit

Cytokines regulate matrix metalloproteinases and migration in cardiac fibroblasts

Inhibition of Matrix Metalloproteinase Activity by TIMP-1 Gene Transfer Effectively Treats Ischemic Cardiomyopathy

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