Collagen chain mRNAs in isolated heart cells from young and adult rats*

Eghbali, Mahboubeh; Czaja, Mark J.; Zeydel, Maria; Weiner, Francis R.; Zern, Mark Α.; Seifter, Sam; Blumenfeld, Olga O.

doi:10.1016/s0022-2828(88)80059-2

Cited by 212 publications

(101 citation statements)

References 30 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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“…Interestingly, the space left by dead myocytes is filled by granulation tissue composed of several cell types, including macrophages, endothelial cells and fibroblasts (20), and newly synthesized extracellular matrix (ECM) (21,22), which is produced mainly by cardiac fibroblasts (23). This observation implies that cardiac fibroblasts are able to endure and secrete the ECM that constitutes the fibrotic scar under situations that threaten survival of other cell types.…”

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confidence: 99%

Bcl-2 Is a Key Factor for Cardiac Fibroblast Resistance to Programmed Cell Death

Mayorga

Bahí

Ballester

et al. 2004

Journal of Biological Chemistry

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Cardiac fibroblasts play an essential role in the physiology of the heart. These produce extracellular matrix proteins and synthesize angiogenic and cardioprotective factors. Although fibroblasts of cardiac origin are known to be resistant to apoptosis and to remain metabolically active in situations compromising cell survival, the underlying mechanisms are unknown. Here, we report that cardiac fibroblasts were more resistant than dermal or pulmonary fibroblasts to mitochondriadependent cell death. Cytochrome c release was blocked in cardiac fibroblasts but not in dermal fibroblasts treated with staurosporine, etoposide, serum deprivation, or simulated ischemia, precluding caspase-3 activation and DNA fragmentation. Resistance to apoptosis of cardiac fibroblasts correlated with the expression of the anti-apoptotic protein Bcl-2, whereas skin and lung fibroblasts did not express detectable levels of this protein. Bcl-x L, Bax, and Bak were expressed at similar levels in cardiac, dermal, and lung fibroblasts. In addition, the death of cardiac fibroblasts during hypoxia was not associated with the cleavage of Bid but rather with Bcl-2 disappearance, suggesting the requirement of the mitochondrial apoptotic machinery to execute death receptor-induced programmed cell death. Knockdown of bcl-2 expression by siRNA in cardiac fibroblasts increased their apoptotic response to staurosporine, serum, and glucose deprivation and to simulated ischemia. Moreover, dermal fibroblasts overexpressing Bcl-2 achieved a similar level of resistance to these stimuli as cardiac fibroblasts. Thus, our data demonstrate that Bcl-2 is an important effector of heart fibroblast resistance to apoptosis and highlight a probable mechanism for promoting survival advantage in fibroblasts of cardiac origin.

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“…[11][12][13][14] Accordingly, we serially measured serum products collagen types I and III turnover, which constitute the bulk of cardiac ECCM, 15 and LV volumes and function in a consecutive sample of patients successfully treated with primary percuta-neous coronary intervention (PCI) for a first AMI with LV systolic dysfunction. The purpose of this study was to evaluate if a different pattern of ECCM and LV remodelling is present in patients with antecedent hypertension compared with those without hypertension.…”

Section: Introductionmentioning

confidence: 99%

Time course of serum collagen types I and III metabolism products after reperfused acute myocardial infarction in patients with and without systemic hypertension

et al. 2008

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We examined 55 consecutive patients successfully treated with primary percutaneous coronary intervention (PCI) for a first acute myocardial infarction with left ventricular (LV) systolic dysfunction. In all patients we performed echocardiographic examination, dosage of plasma brain natriuretic peptide, serum carboxy-terminal propeptide and telopeptide of procollagen type I and amino-terminal propeptide of procollagen type III at days 1 and 3, and at 1 and 6 months after index infarction. The hypertensive patients (group 1; n ¼ 30) differed for higher baseline blood pressure (133±4 mm Hg vs 118±4 mm Hg; P ¼ 0.03), greater LV mass index (108 ± 5 vs 94 ± 4 g m À2 , P ¼ 0.03) and lower mitral E/A wave peak (0.8 ± 0.06 vs 1.1±0.12, P ¼ 0.02) with respect to non-hypertensive patients (group 2; n ¼ 25). From day 1 to month 6 carboxy-terminal propeptide of procollagen type I and amino-terminal propeptide of procollagen type III increased (Po0.005 and Po0.05, respectively) in both groups, whereas carboxy-terminal telopeptide of procollagen type I increased from day 1 to day 3 (Po0.01 in both groups, respectively) and then decreased from day 3 to month 6 (Po0.01 and Po0.05 in both groups, respectively). From day 1, brain natriuretic peptide decreased in both groups (Po0.005). There was no significant difference between the two groups in values of procollagens and natriuretic peptide. Finally, LV diastolic volume and function at 6 months were similar in the two groups. Thus, in patients with reperfused acute myocardial infarction and LV dysfunction, antecedent hypertension was not associated with a different pattern of serum procollagen release and ventricular remodelling at 6 months of follow-up.

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Collagen chain mRNAs in isolated heart cells from young and adult rats*

Cited by 212 publications

References 30 publications

Ventricular Remodeling After Infarction and the Extracellular Collagen Matrix

Ventricular Remodeling After Infarction and the Extracellular Collagen Matrix

Bcl-2 Is a Key Factor for Cardiac Fibroblast Resistance to Programmed Cell Death

Time course of serum collagen types I and III metabolism products after reperfused acute myocardial infarction in patients with and without systemic hypertension

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