Myocardial beta-adrenergic receptor expression and signal transduction after chronic volume-overload hypertrophy and circulatory congestion.

Hammond, H. Kirk; Roth, David A.; Insel, P A; Ford, Charles E.; White, F C; Maisel, AS; Ziegler, Michael G.; Bloor, C. M.

doi:10.1161/01.cir.85.1.269

Cited by 56 publications

(24 citation statements)

References 29 publications

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“…In humans, reduced ␤ 1 -AR mRNA levels (48) and ␤-receptor density (49) are also detected in a mild form of cardiac dysfunction, indicating that down-regulation of ␤-AR receptors is not restricted to severe or advanced heart disease. Moreover, histological analysis of cardiac tissue from volumeoverloaded pigs indicates that decreased responsiveness to ␤-AR stimulation can occur without degenerative changes such as inflammation or fibrosis (50). It is not known at present, however, whether the changes in the ␤-AR system are causes or consequences of heart dysfunction.…”

Section: Discussionmentioning

confidence: 99%

Lack of type XV collagen causes a skeletal myopathy and cardiovascular defects in mice

Eklund¹

2001

Proceedings of the National Academy of Sciences

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Type XV collagen occurs widely in the basement membrane zones of tissues, but its function is unknown. To understand the biological role of this protein, a null mutation in the Col15a1 gene was introduced into the germ line of mice. Despite the complete lack of type XV collagen, the mutant mice developed and reproduced normally, and they were indistinguishable from their wild-type littermates. However, Col15a1-deficient mice showed progressive histological changes characteristic for muscular diseases after 3 months of age, and they were more vulnerable than controls to exercise-induced muscle injury. Despite the antiangiogenic role of type XV collagen-derived endostatin, the development of the vasculature appeared normal in the null mice. Nevertheless, ultrastructural analyses revealed collapsed capillaries and endothelial cell degeneration in the heart and skeletal muscle. Furthermore, perfused hearts showed a diminished inotropic response, and exercise resulted in cardiac injury, changes that mimic early or mild heart disease. Thus, type XV collagen appears to function as a structural component needed to stabilize skeletal muscle cells and microvessels.T ype XV collagen belongs to the heterogeneous group of non-fibril-forming collagens and is thought to be a homotrimer consisting of three ␣1(XV) collagen chains (1). It is characterized by a central highly interrupted triple helical domain and large N-and C-terminal noncollagenous domains (2-4), and it has been shown to be a chondroitin sulfate proteoglycan (5). Type XV collagen mRNAs are expressed in many tissues, but the highest mRNA levels in the mouse can be detected in the heart and skeletal muscle (4). The protein is shown by immunostaining to have a widespread tissue distribution and has been localized mainly to the basement membrane zones, although it can also be found in the fibrillar collagen matrix of some tissues (6, 7). Its function is not known, however.In terms of primary structure, type XV collagen is highly homologous with type XVIII collagen, and together they form a distinct subgroup among the collagens (1, 3). They have thrombospondin-1 sequence homology in the N terminus, seven homologous collagenous domains, and highly homologous Cterminal noncollagenous domains. Type XVIII collagen is the precursor of endostatin, which has been shown to have a potent antiangiogenic effect (8), and the highest degree of homology between collagen types XV and XVIII involves the C-terminal endostatin sequence. The corresponding fragment in type XV collagen has also been shown to have antiangiogenic activity (9, 10).To understand the biological function and significance of type XV collagen, we generated a mouse strain lacking in ␣1(XV) collagen chains by site-specific Cre-loxP-mediated deletion in embryonic stem (ES) cells (11). The data suggest a structural role for type XV collagen in providing mechanical stability between cells and the extracellular matrix in skeletal muscle fibers and microvessels. Col15a1 deficiency leads to functional rather than struct...

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Section: Discussionmentioning

confidence: 99%

Lack of type XV collagen causes a skeletal myopathy and cardiovascular defects in mice

Eklund¹

2001

Proceedings of the National Academy of Sciences

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“…The presence of enough -adrenergic receptors is necessary to adapt to the increased oxygen demand (Hammond et al, 1992;Figueras & Lindon, 1995). However, the number ofadrenergic receptors decreases if there is volume overload-induced myocardial hypertrophy, or if the endothelial cells of the coronary artery are impaired (Figueras & Lidon, 1995;Hammond et al, 1992).…”

Section: α-And β-Adrenergic Receptor Response Of Coronary Artery Endomentioning

confidence: 99%

“…However, the number ofadrenergic receptors decreases if there is volume overload-induced myocardial hypertrophy, or if the endothelial cells of the coronary artery are impaired (Figueras & Lidon, 1995;Hammond et al, 1992). Patients with unstable angina during bed rest and with significant coronary disease demonstrate a lower ischemic threshold early in the morning (Figueras & Lindon, 1995).…”

Section: α-And β-Adrenergic Receptor Response Of Coronary Artery Endomentioning

confidence: 99%

“…Patients with unstable angina during bed rest and with significant coronary disease demonstrate a lower ischemic threshold early in the morning (Figueras & Lindon, 1995). Usually, plasma levels of norepinephrine are increased and myocardial levels of norepinephrine are decreased in patients with fewer -adrenergic receptors (West, 1990;Hammond et al, 1992). The increased plasma norepinephrine overstimulates sympathetic nervous activity and acts mostly on -adrenergic receptors, causing vessel constriction ( Hammond et al, 1992;Kuo et al, 1993;West, 1990).…”

Section: α-And β-Adrenergic Receptor Response Of Coronary Artery Endomentioning

confidence: 99%

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Theoretical Identification of Behavioral Risk Factors Among Multiple Risk Factors Causing Morning Onset of Cardiac Events due to Circadian Variations

Furukawa¹,

Morimoto²

2012

Recent Advances in Cardiovascular Risk Factors

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“…Several lines of evidence suggest that one or more G proteins may be altered in certain cardiac disease states. Among the animal models of chronic heart failure, dogs with pressure-overload cardiac hypertrophy and pigs with volume-overload cardiac hypertrophy have shown evidence of decreased G sα in myocardial membranes (Longabaugh et al 1988;Hammond et al 1992). In the cardiomyopathic Syrian hamster, a loss of G sα function but not a quantitative loss of G sα protein or its mRNA has been demonstrated (Kessler et al 1989).…”

Section: Introductionmentioning

confidence: 99%

Differential gene transcriptional regulation of Gi isoforms and Gs protein expression in diabetic rat hearts

Matsuda

Hattori

Gando

et al. 2000

Naunyn-Schmiedeberg's Arch Pharmacol

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Many cardiac diseases can be associated with alterations in the function and quantity of G proteins. We examined the gene expressions and protein levels of Gi-1alpha, Gi-2alpha, Gi-3alpha and G(s alpha) in ventricular myocardial preparations from rats 4-6 weeks after induction of diabetes with streptozotocin in comparison with those from age-matched control rats. Diabetic rat myocardium exhibited reductions in the protein levels of Gi-2alpha and Gi-3alpha by 22+/-2% and 57+/-2%, respectively. In diabetes, 22% and 53% reductions in myocardial mRNA levels of Gi-2alpha and Gi-3alpha were observed. Although a faint protein signal of Gi-1alpha was detectable, no apparent expression of mRNA for Gi-1alpha was found in either control or diabetic myocardium. The reduced protein and mRNA levels of Gi-2alpha and Gi-3alpha were prevented by insulin therapy. No change was found in the protein and mRNA levels of G(s alpha) in diabetic myocardium. In conclusion, diabetes leads to a differential regulation of protein expressions of G(i alpha) isoforms and G(s alpha) in ventricular myocardium. The reduced expression of Gi-2alpha and Gi-3alpha proteins can be explained, at least in part, by the decreases in the transcriptional levels.

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Myocardial beta-adrenergic receptor expression and signal transduction after chronic volume-overload hypertrophy and circulatory congestion.

Cited by 56 publications

References 29 publications

Lack of type XV collagen causes a skeletal myopathy and cardiovascular defects in mice

Lack of type XV collagen causes a skeletal myopathy and cardiovascular defects in mice

Theoretical Identification of Behavioral Risk Factors Among Multiple Risk Factors Causing Morning Onset of Cardiac Events due to Circadian Variations

Differential gene transcriptional regulation of Gi isoforms and Gs protein expression in diabetic rat hearts

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