Localization of types I, III and IV collagen mRNAs in rat heart cells by in situ hybridization

Eghbali, Mahboubeh; Blumenfeld, Olga O.; Seifter, Sam; Buttrick, Peter M.; Leinwand, Leslie A.; Robinson, Thomas F.; Zern, Mark Α.; Giambrone, M. A.

doi:10.1016/0022-2828(89)91498-3

Cited by 204 publications

(93 citation statements)

References 18 publications

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“…First, the LV remodeling process after MI is complex, dynamic, and time dependent, and progresses in parallel with healing over months. 1,2,7,16 Notably, it involves differential changes between the IZ and NIZ with respect to the following: (1) LV structure, shape, and topography 1,2 ( Figure 1); (2) cell type, such as myocytes and nonmyocytes (Table 1) 6,7,[17][18][19][20][21][22][23] ; (3) proteins, cytokines, and growth factors 7,24,25 ; and (4) the ECCM. 5-7,13-17,19 -23 Differential regional remodeling of the ECCM contributes significantly to global LV structural remodeling after MI ( Figure 2) 7,9,26 and plays a pivotal role in paradigm 1.…”

Section: Ventricular Remodeling After MI and The Role Of Eccmmentioning

confidence: 99%

“…33,38 In reperfused MI, decreased or damaged ECCM in the IZ 5,12,39 is associated with cardiac rupture. 5,39 Key Points to Remember About Pathobiology of Cardiac ECCM First, nearly 75% of the cells in the healthy heart are nonmyocytes, which include fibroblasts 18,21 that account for 90% to 95% of nonmyocyte cell mass 17,20,21 (Table 1). Myocardial cells are supported by a matrix (Table 4) consisting of a macromolecular network of fibers 36 with intricate 3D organization 11 that largely determines the structural and functional integrity of the heart.…”

Section: Ventricular Remodeling After MI and The Role Of Eccmmentioning

confidence: 99%

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Ventricular Remodeling After Infarction and the Extracellular Collagen Matrix

2003

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L eft ventricular (LV) remodeling after myocardial infarction (MI) contributes significantly to LV dilation and dysfunction, and disability and death. Two paradigms, pertinent to antiremodeling therapy after MI (Figure 1), have evolved over the last 3 decades. Paradigm 1, LV remodeling is a major mechanism for disability and death, 1,2 has received a great deal of attention. In contrast, paradigm 2, remodeling of the extracellular collagen matrix (ECCM) plays a major role in LV remodeling, [3][4][5][6][7] whereby decrease, disruption, and/or defective composition of the ECCM promote LV dilation and rupture, 4 -7 has received little attention. A host of clinical trials showed that angiotensin-converting enzyme (ACE) inhibitors (ACE-Is) with or without aldosterone antagonists, angiotensin II (AngII) type 1 (AT 1 ) receptor blockers (ARBs), ␤-adrenergic blockers or reperfusion improve outcome in survivors of MI. 8 -10 Concurrent evidence has underscored the importance of preserving the ECCM during healing after MI. [2][3][4][5][6][7] However, the antifibrotic action of ACE-Is, aldosterone antagonists and ARBs on ECCM in the infarct zone (IZ) and noninfarct zone (NIZ), 6,7,9,11 and the reperfusion-induced damage to the ECCM in the IZ, 5,7,12 remain unreconciled with the benefits. 8 -10,13 Nevertheless, excessive ECCM, as in dilated ischemic cardiomyopathy after remote MI, 14,15 can contribute to LV diastolic dysfunction and poor outcome, 6 suggesting that antifibrotic drugs that target excess ECCM might be a logical therapeutic approach. This review focuses on the role of the ECCM in the evolution of LV remodeling after MI and the potential impact of therapies that target the ECCM. Ventricular Remodeling After MI and the Role of ECCMFive points merit emphasis. First, the LV remodeling process after MI is complex, dynamic, and time dependent, and progresses in parallel with healing over months. 1,2,7,16 Notably, it involves differential changes between the IZ and NIZ with respect to the following: (1) LV structure, shape, and topography 1,2 ( Figure 1); (2) cell type, such as myocytes and nonmyocytes (Table 1) 6,7,[17][18][19][20][21][22][23] ; (3) proteins, cytokines, and growth factors 7,24,25 ; and (4) the ECCM. 5-7,13-17,19 -23 Differential regional remodeling of the ECCM contributes significantly to global LV structural remodeling after MI (Figure 2) 7,9,26 and plays a pivotal role in paradigm 1. 3,6,7 Second, the post-MI heart shows remarkable capacity to adapt to the rather sudden development of an IZ and a NIZ. Thus, MI results in time-dependent damage to myocytes, nonmyocytes, and the ECCM in the IZ; ventricular dysfunction followed by volume overload and progressive dilation; reactive hypertrophy with interstitial fibrosis and increased collagen in the NIZ; gradual reparative fibrosis in the IZ 27 ; and vascular remodeling in the IZ and NIZ. 7 Third, several endogenous molecules that affect collagen synthesis and are upregulated after MI, and several agents that are used therapeutically for MI, affect co...

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Section: Ventricular Remodeling After MI and The Role Of Eccmmentioning

confidence: 99%

Section: Ventricular Remodeling After MI and The Role Of Eccmmentioning

confidence: 99%

Ventricular Remodeling After Infarction and the Extracellular Collagen Matrix

2003

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“…76 Type I collagen predominates in both the normal and diseased heart. Cardiac fibroblasts contain the mRNAs for types I and III collagen, 77 and therefore these cells or fibroblast-like cells are probably responsible for the fibrous tissue responses found in the myocardium.…”

Section: Cardiac Fibroblast Collagen Turnovermentioning

confidence: 99%

Structural remodeling in hypertensive heart disease and the role of hormones.

1994

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In hypertension, the risk of adverse cardiovascular events, including heart failure, is increased in the presence of left ventricular hypertrophy. Morphological studies suggest that it is not the quantity but rather the quality, or structure, of myocardium that confers such risk. Iterations in tissue structure that appear in hypertensive heart disease include a remodeling of intramyocardial coronary arterioles, similar to that found in systemic organs, and a disproportionate accumulation of fibrillar collagen within their adventitia and neighboring interstitial space. Microscopic scars replacing necrotic cardiac myocytes are also evident. These expressions of fibrosis appear in the normotensive, nonhypertrophied right and hypertensive, hypertrophied left ventricles and are linked to the renin-angiotensin-aldosterone system. Cardiac myocyte growth, the major determinant of myocardial mass, is related to ventricular loading. Mechanisms responsible for the reactive and reparative fibrosis with renin-angiotensin-aldosterone system activation are under investigation. In vitro quantitative autoradiography has identified angiotensin II, aldosterone, T he appearance of symptomatic heart failure and adverse cardiovascular events, such as myocardial infarction, sudden cardiac death, and stroke, occur with increased frequency in patients with systemic hypertension. For years, the pathophysiologica] basis for such increased risk has been presumed to be solely related to elevated arterial pressure. More recently, emphasis in conferring risk has been placed on the structural remodeling of the cardiovasculature. For example, in patients with uncomplicated hypertension, risk has been linked to left ventricular hypertrophy (LVH). 13 Viewed not as a separate organ but as an integral component of the cardiovasculature, the heart and its intramyocardial coronary arteries and arterioles participate in a structural remodeling that involves systemic organs as well. 48 The remodeling of systemic arterioles accounts for hypertension. The heart in turn responds to enhanced ventricular loading with a hypertrophic growth of cardiac myocytes, and accordingly, left ventricular mass is increased. The diffuse nature of the structural remodeling process, involving the right and left ventricles and systemic organs, suggests a role for circulating substances or substances produced locally within cardiovascular tissue. In this connection, it is noteworthy that risk has also been linked to an activation of the renin-angiotensin-aldosterone system (RAAS). endothelin, and bradykinin receptors in the myocardium. A nonendothelial tissue angiotensin-converting enzyme, whose binding density is marked in the matrix of heart valves, adventitia, and sites of fibrosis, irrespective of its pathogenic basis, has also been found. This angiotensin-converting enzyme may be responsible for regulating local concentrations of angiotensin II and bradykinin that govern fibroblast collagen turnover. Based on a paradigm of discordant reciprocal regulation, in wh...

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“…The ma-trix provides structural support and facilitates ventricular function in response to changes in mechanical forces within the myocardium during the cardiac cycle (Weber et al, 1988(Weber et al, , 1989Eghbali et al, 1989). Dysregulation of collagen fibers is detrimental to myocardial function and increased deposition in the form of fibrosis has been reported in many models of myocardial hypertrophy and cardiac failure (Diez et al, 2005;Baudino et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

“…Several collagen types (I, II, III, V, VI, XI, XXIII) have been identified in distinct compartments of embryonic and adult heart valves and are associated with the differential functions of the valve leaflets vs. the supporting apparatus (Icardo and Colvee, 1995;Hinton et al, 2006;Lincoln et al, 2006b). Specific collagens (I, III, V) also contribute to the fibrous ECM of the ventricular myocardium (Medugorac and Jacob, 1983;Eghbali et al, 1989). These collagens are highly organized to provide a supporting fibrous scaffold able to transmit forces in the myocardium during the cardiac cycle (Baudino et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

ColVa1 and ColXIa1 are required for myocardial morphogenesis and heart valve development

Lincoln

Florer

Deutsch

et al. 2006

Developmental Dynamics

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Genetic mutations in minor fibrillar collagen types Va1 (ColVa1) and XIa1 (ColXI) have been identified in connective tissue disorders including Ehlers-Danlos syndrome and chondrodysplasias. ColVa1؉/؊ and ColXIa1؊/؊ mutant mice recapitulate these human disorders and show aberrations in collagen fiber organization in connective tissue of the skin, cornea, cartilage, and tendon. In the heart, fibrous networks of collagen fibers form throughout the ventricular myocardium and heart valves, and alterations in collagen fiber homeostasis are apparent in many forms of cardiac disease associated with myocardial dysfunction and valvular insufficiency. There is increasing evidence for cardiac dysfunction in connective tissue disorders, but the mechanisms have not been addressed. ColVa1؉/؊ and ColXIa1؊/؊ mutant mice were used to identify roles for ColVa1 and ColXIa1 in ventricular myocardial morphogenesis and heart valve development. These affected cardiac structures show a compensatory increase in type I collagen deposition, similar to that previously described in valvular and cardiomyopathic disease. Morphological cardiac defects associated with changes in collagen fiber homeostasis identified in ColVa1؉/؊ and ColXIa1؊/؊ mice provide an insight into previously unappreciated forms of cardiac dysfunction associated with connective tissue disorders. Developmental Dynamics 235:3295-3305, 2006.

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Localization of types I, III and IV collagen mRNAs in rat heart cells by in situ hybridization

Cited by 204 publications

References 18 publications

Ventricular Remodeling After Infarction and the Extracellular Collagen Matrix

Ventricular Remodeling After Infarction and the Extracellular Collagen Matrix

Structural remodeling in hypertensive heart disease and the role of hormones.

ColVa1 and ColXIa1 are required for myocardial morphogenesis and heart valve development

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