Molecular dynamics of the compensatory response to myocardial infarct

LaFramboise, William A.; Bombach, Kelly L.; Dhir, Rajiv; Muha, Noah; Cullen, R.F.; Pogozelski, Andrew R.; Türk, Dóra; George, Joshy; Guthrie, Robert D.; Magovern, James A.

doi:10.1016/j.yjmcc.2004.09.011

Cited by 45 publications

(40 citation statements)

References 22 publications

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“…Finally, this is accompanied by a shift from a predominantly aerobic metabolism to a more anaerobic glycolytic metabolism, which allows a better regulation of the recovery period of the contractile cycle. Such a shift has been further confirmed by large-scale analysis of gene expression (LaFramboise et al, 2005). In acute conditions, mechanical overload worsens the thermodynamic conditions and can immediately produce acute failure.…”

Section: Global Increase In Expressionmentioning

confidence: 78%

“…Several studies have been published using such a technology; some, in human, were pilot feasibility studies (Steenman et al, 2005) and others, using rats after myocardial infarction, were more complete (LaFramboise et al, 2005). Fourteen recent study reports pertaining to gene array analysis have been reviewed (Sharma et al, 2005).…”

Section: Gene Reprogrammingmentioning

confidence: 99%

“…Nevertheless, finally, the cardiac response to mechanics involves changes in expression, including allelic modifications that reproduce the foetal programme (Lompré, 1979). Cardiac remodelling involves the whole organ and genome-wide analyses have revealed significant coordinated changes in over 1400 genes early and 125 genes late in the infarct zone, and nearly 600 genes early and 100 genes late in the non-infarct zone (LaFramboise et al, 2005). As such, it resembles yeast remodelling in response to various changes in the extracellular environment.…”

Section: Transition To Heart Failurementioning

confidence: 99%

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Phenotypic plasticity of adult myocardium: molecular mechanisms

Swynghedauw

2006

Journal of Experimental Biology

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Molecular cardiologists, even clinical cardiologists, are familiar with phenotypic plasticity. They call it remodelling*. Myocardial and vascular remodelling have primarily a mechanical origin and an adaptive significance. Cardiac remodelling (CR) occurs in response to chronic mechanical overloading, and arterial remodelling is a response to permanent arterial hypertension (Lompré et al., 1979;Swynghedauw, 1999;Levy and Tedgui, 1999). CR leads to heart failure and, with cancer, is one of the major causes of death in our countries, so cardiac plasticity is a major public health problem. This review will only focus on myocardial remodelling (excluding the remodelling of coronary vessels).This review will start from the most common clinical conditions † , namely CR occurring after myocardial infarction or chronic essential arterial hypertension, and will consider Cardiac phenotypic plasticity (so-called cardiac remodelling, CR) is characterized by changes in myocardial structure that happen in response to either mechanical overload or a loss of substance such as that occurring after myocardial infarction.Mechanosensation is a widespread biological process and is inextricably mixed with other transduction systems from hormones and vasopeptides, which ultimately produce post-translational modifications of transcription factors. The expression of the four main transcription factors during cardiogenesis is also enhanced as a link to foetal reprogramming.CR results from re-expression of the foetal programme, which is mostly adaptive, but also from several other phenotypic modifications that are not usually adaptive, such as fibrosis. (i) The initial determinant is mechanical, and reexpression of the foetal programme includes a global increase in genetic expression with cardiac hypertrophy, reexpression of genes that are normally not expressed in the adult ventricles, repression of genes not expressed during the foetal life, and activation of pre-exisiting stem cells. Microarray technology has revealed a coordinated change in expression of genes pertaining to signal transduction, metabolic function, structure and motility, and cell organism defence. The physiological consequence is a better adapted muscle. (ii) During clinical conditions, the effects of mechanics are modified by several interfering determinants that modify CR, including senescence, obesity, diabetes, ischemia and the neurohormonal reaction. Each of these factors can alter myocardial gene expression and modify molecular remodelling of mechanical origin.Finally, as compared to evolutionary phenotypic plasticity described in plants and insects in response to variations in environmental conditions, in CR, the environmental factor is internal, plasticity is primarily adaptive, and it involves coordinated changes in over 1400 genes. Study of reaction norms showed that the genotypes from different animal species are similarly plastic, but there are transgenic models in which adaptation to mechanics is not caused by hypertrophy but by qualitative changes in gene...

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Section: Global Increase In Expressionmentioning

confidence: 78%

Section: Gene Reprogrammingmentioning

confidence: 99%

Section: Transition To Heart Failurementioning

confidence: 99%

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Phenotypic plasticity of adult myocardium: molecular mechanisms

Swynghedauw

2006

Journal of Experimental Biology

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“…remodeling process within the viable (noninfarcted) myocardium (4,21,46). The tissue used in the microarray analysis was LV tissue consisting of a heterogenous population of cell types; thus, the origin of the expressional changes seen may represent cell infiltration, especially those relating to the immune response.…”

Section: Discussionmentioning

confidence: 99%

The myocardial contractile response to physiological stress improves with high saturated fat feeding in heart failure

Berthiaume¹,

Bray²,

McElfresh³

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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Berthiaume JM, Bray MS, McElfresh TA, Chen X, Azam S, Young ME, Hoit BD, Chandler MP. The myocardial contractile response to physiological stress improves with high saturated fat feeding in heart failure. Am J Physiol Heart Circ Physiol 299: H410 -H421, 2010. First published May 28, 2010 doi:10.1152/ajpheart.00270.2010.-Impaired myocardial contractile function is a hallmark of heart failure (HF), which may present under resting conditions and/or during physiological stress. Previous studies have reported that high fat feeding in mild to moderate HF/left ventricular (LV) dysfunction is associated with improved contractile function at baseline. The goal of this study was to determine whether myocardial function is compromised in response to physiological stress and to evaluate the global gene expression profile of rats fed high dietary fat after infarction. Male Wistar rats underwent ligation or sham surgery and were fed normal chow (NC; 10% kcal fat; Sham ϩ NC and HF ϩ NC groups) or high-fat chow (SAT; 60% kcal saturated fat; Sham ϩ SAT and HF ϩ SAT groups) for 8 wk. Myocardial contractile function was assessed using a Millar pressure-volume conductance catheter at baseline and during inferior vena caval occlusions and dobutamine stress. Steady-state indexes of systolic function, LV ϩdP/dt max, stroke work, and maximal power were increased in the HF ϩ SAT group versus the HF ϩ NC group and reduced in the HF ϩ NC group versus the Sham ϩ NC group. Preload recruitable measures of contractility were decreased in HF ϩ NC group but not in the HF ϩ SAT group. ␤-Adrenergic responsiveness [change in LV ϩdP/dt max and change in cardiac output with dobutamine (0 -10 g·kg Ϫ1 ·min Ϫ1 )] was reduced in HF, but high fat feeding did not further impact the contractile reserve in HF. The contractile reserve was reduced by the high-fat diet in the Sham ϩ SAT group. Microarray gene expression analysis revealed that the majority of significantly altered pathways identified contained multiple gene targets correspond to cell signaling pathways and energy metabolism. These findings suggest that high saturated fat improves myocardial function at rest and during physiological stress in infarcted hearts but may negatively impact the contractile reserve under nonpathological conditions. Furthermore, high fat feeding-induced alterations in gene expression related to energy metabolism and specific signaling pathways revealed promising targets through which high saturated fat potentially mediates cardioprotection in mild to moderate HF/LV dysfunction. contractile function; infarction; high-fat diet; gene array analysis CHRONIC DISEASES AND CONDITIONS including obesity, insulin resistance, and diabetes are linked to elevations in plasma free fatty acids (FFA) leading to enhanced lipid accumulation in nonadipose tissue (24). Enhanced myocardial lipid accumulation has been associated with decreases in myocardial contractile function, resulting in the progression of heart failure (HF). Nutritional guidelines from the American Heart Association (2...

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“…MT also appears to be protective against ovalbumin-induced airway inflammation (66). Gene profiling in other pathologies, including experimental models of diabetes (74) and myocardial infarction (75), also has revealed MT as a candidate molecule. MT protein has been shown to be elevated in hyperoxia (2), and indeed its mRNA is used as an index of sensitivity to hyperoxic injury (76).…”

Section: Mt and Lung Biologymentioning

confidence: 99%

Nitric Oxide and Zinc Homeostasis in Acute Lung Injury

Croix

Leelavaninchkul²,

Watkins³

et al. 2005

Proceedings of the American Thoracic Society

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Among putative small molecules that affect sensitivity to acute lung injury, zinc and nitric oxide are potentially unique by virtue of their interdependence and dual capacities to be cytoprotective or injurious. Nitric oxide and zinc appear to be linked via an intracellular signaling pathway involving S-nitrosation of metallothoineinitself a small protein known to be an important inducible gene product that may modify lung injury. In the present article, we summarize recent efforts using genetic and fluorescence optical imaging techniques to: (1 ) demonstrate that S-nitrosation of metallothionein affects intracellular zinc homeostasis in intact pulmonary endothelial cells; and (2 ) reveal a protective role for this pathway in hyperoxic and LPS-induced injury.

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Molecular dynamics of the compensatory response to myocardial infarct

Cited by 45 publications

References 22 publications

Phenotypic plasticity of adult myocardium: molecular mechanisms

Phenotypic plasticity of adult myocardium: molecular mechanisms

The myocardial contractile response to physiological stress improves with high saturated fat feeding in heart failure

Nitric Oxide and Zinc Homeostasis in Acute Lung Injury

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