Viscoelastic properties of pressure overload hypertrophied  myocardium: effect of serine protease treatment

Stroud, Jason D.; Baicu, Catalin F.; Barnes, Michael C.; Spinale, Francis G.; Zile, Michael R.

doi:10.1152/ajpheart.00711.2001

Cited by 60 publications

(44 citation statements)

References 42 publications

(106 reference statements)

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“…33 Degradation of collagen in pressure-overloaded, hypertrophied papillary muscles with plasmin did not reduce muscle stiffness to levels observed in normal muscles. 34 Similarly, in the present study, patients with DHF and low CVFs still had higher LVEDP, , and E than did controls (Figure 3). Therefore, our data support the concept that diastolic LV dysfunction in the presence of a low CVF is explained by the higher F passive of the cardiomyocytes.…”

Section: In Vitro Versus In Vivosupporting

confidence: 78%

Cardiomyocyte Stiffness in Diastolic Heart Failure

Borbély¹,

Velden²,

Papp³

et al. 2005

Circulation

469

386

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Background-Heart failure with preserved left ventricular (LV) ejection fraction (EF) is increasingly recognized and usually referred to as diastolic heart failure (DHF). Its pathogenetic mechanism remains unclear, partly because of a lack of myocardial biopsy material. Endomyocardial biopsy samples obtained from DHF patients were therefore analyzed for collagen volume fraction (CVF) and sarcomeric protein composition and compared with control samples. Single cardiomyocytes were isolated from these biopsy samples to assess cellular contractile performance. Methods and Results-DHF patients (nϭ12) had an LVEF of 71Ϯ11%, an LV end-diastolic pressure (LVEDP) of 28Ϯ4 mm Hg, and no significant coronary artery stenoses. DHF patients had higher CVFs (7.5Ϯ4.0%, PϽ0.05) than did controls (nϭ8, 3.8Ϯ2.0%), and no conspicuous changes in sarcomeric protein composition were detected. Cardiomyocytes, mechanically isolated and treated with Triton X-100 to remove all membranes, were stretched to a sarcomere length of 2.

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Section: In Vitro Versus In Vivosupporting

confidence: 78%

Cardiomyocyte Stiffness in Diastolic Heart Failure

Borbély¹,

Velden²,

Papp³

et al. 2005

Circulation

469

386

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“…Because excessive accumulation of collagen in the cardiac interstitium is associated with pressure-overload hypertrophy, we speculate that myofibroblast conversion and the accompanying increase in collagenous ECM deposition by myofibroblasts contributes to increased amounts of collagen (24,42). Overdeposition of collagen in the heart has been associated with cardiac dysfunction, particularly in respect to relaxation of the ventricles during diastole (33,44). Potentially, a distinct ECM synthesized by myofibroblasts could induce changes in integrin-mediated cell signaling, display different susceptibility to collagenase digestion by matrix metalloproteinases, and/or exhibit disparate structural properties.…”

Section: Discussionmentioning

confidence: 99%

Cardiac myofibroblasts differentiated in 3D culture exhibit distinct changes in collagen I production, processing, and matrix deposition

Poobalarahi¹,

Baicu²,

Bradshaw³

2006

American Journal of Physiology-Heart and Circulatory Physiology

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Myofibroblasts are a differentiated fibroblast cell type characterized by increased contractile capacity and elevated production of extracellular matrix (ECM) proteins. In the heart, myofibroblast expression is implicated in fibrosis associated with pressure-overload hypertrophy, among other pathologies. Although enhanced expression of ECM proteins by myofibroblasts is established, few studies have addressed the nature of the ECM deposited by myofibroblasts. To characterize ECM production and assembly by cardiac myofibroblasts, we developed a threedimensional (3D) culture system using primary cardiac fibroblasts seeded into a nylon mesh that allows us to reversibly interconvert between myofibroblast and fibroblast phenotypes. We report that an increase in collagen I production by myofibroblasts was accompanied by a significant increase in collagen deposition into insoluble ECM. Furthermore, myofibroblasts exhibited increased levels of procollagen ␣1(I) with C-propeptide attached (and N-propeptide removed) relative to procollagen ␣1(I) compared with fibroblast cultures. An increase in production of the myofibroblast-associated splice variant of fibronectin (EDA-Fn) was seen in myofibroblast 3D cultures. Because the regulation of procollagen I processing is known to have profound effects on ECM assembly, differences in procollagen I secretion and maturation coupled with expression of EDA-Fn are shown to contribute to the production of a distinct ECM by the cardiac myofibroblast.

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“…In POH, the accumulation of ECM and eventual myocardial fibrosis significantly contributes to LV function. In particular, enhanced synthesis and deposition of myocardial ECM is directly associated with increased LV myocardial stiffness properties, which in turn causes poor filling characteristics during diastole (12,35,159,191,194,312,314,421,488). Indeed, recent clinical evidence suggests that progressive ECM accumulation and diastolic dysfunction are important underlying pathophysiological mechanisms for heart failure in patients with POH (196,544,545).…”

Section: Myocardial Remodeling In Overload Statesmentioning

confidence: 99%

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Spinale¹

2007

Physiological Reviews

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1,023

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It is now becoming apparent that dynamic changes occur within the interstitium that directly contribute to adverse myocardial remodeling following myocardial infarction (MI), with hypertensive heart disease and with intrinsic myocardial disease such as cardiomyopathy. Furthermore, a family of matrix proteases, the matrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs), has been recognized to play an important role in matrix remodeling in these cardiac disease states. The purpose of this review is fivefold: 1) to examine and redefine the myocardial matrix as a critical and dynamic entity with respect to the remodeling process encountered with MI, hypertension, or cardiomyopathic disease; 2) present the remarkable progress that has been made with respect to MMP/TIMP biology and how it relates to myocardial matrix remodeling; 3) to evaluate critical translational/clinical studies that have provided a cause-effect relationship between alterations in MMP/TIMP regulation and myocardial matrix remodeling; 4) to provide a critical review and analysis of current diagnostic, prognostic, and pharmacological approaches that utilized our basic understanding of MMP/TIMPs in the context of cardiac disease; and 5) most importantly, to dispel the historical belief that the myocardial matrix is a passive structure and supplant this belief that the regulation of matrix protease pathways such as the MMPs and TIMPs will likely yield a new avenue of diagnostic and therapeutic strategies for myocardial remodeling and the progression to heart failure.

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Viscoelastic properties of pressure overload hypertrophied myocardium: effect of serine protease treatment

Cited by 60 publications

References 42 publications

Cardiomyocyte Stiffness in Diastolic Heart Failure

Cardiomyocyte Stiffness in Diastolic Heart Failure

Cardiac myofibroblasts differentiated in 3D culture exhibit distinct changes in collagen I production, processing, and matrix deposition

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

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