Hypoxia and glucose independently regulate the beta-adrenergic receptor-adenylate cyclase system in cardiac myocytes.

Rocha‐Singh, Krishna; Honbo, Norman; Karliner, Joel S.

doi:10.1172/jci115279

Cited by 32 publications

(15 citation statements)

References 61 publications

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“…LDH release from glucose-supplemented myocytes subjected to 2 h of hypoxia and from glucose-deprived myocytes subjected to 30 or 60 min of hypoxia was no different from normoxic control cells (24). These data suggested that hypoxic preconditioning does not cause irreversible cellular damage, an assumption that we verified using a cell viability assay (see below).…”

Section: Methodssupporting

confidence: 68%

“…Lactate Dehydrogenase Assay-The effect of hypoxia on LDH release from cardiac myocytes was assessed as described previously (24). Following each treatment, culture media were stored at 4°C.…”

Section: Methodsmentioning

confidence: 99%

“…A 30-min hypoxic period was chosen for preconditioning because it was both long enough to induce ⑀PKC activation (Fig. 5C, left) and brief enough to preserve cell viability (24). We found that single-cycle hypoxic preconditioning in glucose-free defined medium increased the proportion of surviving myocytes by 86% compared with control (66.4 Ϯ 1.9 versus 37.9 Ϯ 2.5%) following 9 h of hypoxia.…”

Section: Characteristics Of the Hypoxic Preconditioning Model-ourmentioning

confidence: 95%

“…The hypoxic period was based on our observation that myocytes incubated in glucose-supplemented medium tolerated up to 2 h of hypoxia without reduction of viability (24). The number of cycles was based on the study of preconditioning in canine myocardium in which four brief coronary artery occlusions protected cardiac tissue from prolonged ischemia (1).…”

Section: Characteristics Of the Hypoxic Preconditioning Model-ourmentioning

confidence: 99%

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A Selective ε-Protein Kinase C Antagonist Inhibits Protection of Cardiac Myocytes from Hypoxia-induced Cell Death

Gray

Karliner

Mochly‐Rosen

1997

Journal of Biological Chemistry

369

307

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Protein kinase C activation is thought to protect cardiac tissue from subsequent ischemic injury by a process termed preconditioning. The protein kinase C isozyme that mediates preconditioning has not yet been identified. Using a cell culture model of hypoxic preconditioning, we found that cardiac myocyte viability after 9 h of hypoxia was increased by more than 50% over control. Preconditioning activated protein kinase C isozymes as evidenced by translocation from one cell compartment to another as follows: there was a 2.1-fold increase in ⑀-protein kinase C activation, a 2.8-fold increase in ␦-protein kinase C activation, and no increase in ␤ I -protein kinase C activation. 4␤-Phorbol 12-myristate 13-acetate mimicked hypoxic preconditioning, increasing myocyte survival after prolonged hypoxia by 34% compared with control. We previously identified an ⑀-protein kinase C-selective antagonist, ⑀V1-2 peptide, that inhibits ⑀-protein kinase C translocation and function in cardiac myocytes (Johnson, J. A., Gray, M. O., Chen, C.-H., and Mochly-Rosen, D. (1996) J. Biol. Chem. 271, 24962-24966). ⑀V1-2 peptide abolished hypoxic preconditioning and phorbol ester-mediated cardiac protection. Therefore, preconditioning can be induced in this culture model, and activation of ⑀-protein kinase C is critical for cardiac myocyte protection.

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Section: Methodssupporting

confidence: 68%

Section: Methodsmentioning

confidence: 99%

Section: Characteristics Of the Hypoxic Preconditioning Model-ourmentioning

confidence: 95%

Section: Characteristics Of the Hypoxic Preconditioning Model-ourmentioning

confidence: 99%

See 2 more Smart Citations

A Selective ε-Protein Kinase C Antagonist Inhibits Protection of Cardiac Myocytes from Hypoxia-induced Cell Death

Gray

Karliner

Mochly‐Rosen

1997

Journal of Biological Chemistry

369

307

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“…In congenital heart diseases, cyanosis has been associated with various alterations in cardiac sympathetic activity (1)(2)(3)(4)(5)(6). In acute hypoxemia, for example, stimulation of the sympathetic activity results in increased heart rate and cardiac output as a compensatory mechanism to maintain adequate oxygen supply (7,8), whereas in chronic situations, such as in cyanotic congenital heart disease, several complex events probably contribute toward the mechanism(s) to sustain adequate oxygen supply (9).…”

mentioning

confidence: 99%

Regulation of Sympathetic Activity in Children with Various Congenital Heart Diseases

Dzimiri¹,

Galal

Moorji³

et al. 1995

Pediatr Res

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We studied the a-and P-adrenoceptor activity and catecholamine and cAMP levels in 112 children and infants admitted to the hospital for diagnostic or inte~entional catheterization of tetralogy of Fallot, ventricular septa1 defects with or without hypertension, pulmonary stenosis, coarctation of the aorta, and various complex cyanotic congenital cardiac diseases and compared them with 14 children undergoing transcatheter occlusion of patent ductus arteriosus with insignificant left-to-right-shunts. The mean total platelet a-adrenoceptor density of the study population was elevated by 73%. Both the increases in acyanotic ( p < 0.05) and cyanotic ( p < 0.005) patients as well as the difference between the two groups ( p < 0.01) were significant.Based on the congenital disease classification, the elevation in receptor density was also significant in all groups of patients, except coarctation of the aorta. On the other hand, the mean lymphocyte P-adrenoceptor density was attenuated by 27%, showing significant difference between the acyanotic and the patent ductus arteriosus groups, but none between acyanotic and cyanotic or cyanotic and the patent ductus arteriosus groups. Among the congenital groups, only the left-to-right shunts and the pulmonary stenosis group showed significant ( p < 0.05) decrease in P-adrenoceptor density, whereas the affinity of all the groups toward [125~]iodocyanopindolol was hardly influenced. The plasma levels of all three catecholamines, norepinephrine, epinephrine, and dopamine, were elevated, but cAMP remained unchanged. It seems that the sympathetic nervous system responds to changes triggered by some congenital heart diseases by stimulating a-adrenoceptors, which may be further increased by cyanosis and an attenuation of P-adrenoceptors associated with an increase in plasma catecholamine levels. (Pediatr Res 38: 55-60, 1995) Abbreviations ACY, acyanotic group CYN, cyanotic group TOF, tetralogy of Fallot LRS, left-to-right shunts PST, pulmonary stenosis COA, coarctation of the aorta CPL, complex cyanotic heart diseases PDA, patent ductus arteriosus QpIQs ratio, ratio of pulmonary blood flow to systemic blood flow

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Signal Transduction in the Cardiovascular System in Health and Disease

Srivastava¹,

Anand‐Srivastava²

2008

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except for brief excerpts in connection with reviews or scholarly analysis. Use in connection with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed is forbidden. The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an expression of opinion as to whether or not they are subject to proprietary rights. Cover illustration:Printed on acid-free paper 9 8 7 6 5 4 3 2 1 springer.com PrefaceIn recent years, there has been a surge of interest in studies related to the role of a variety of signaling pathways in the control of cardiovascular physiology. Evidence has also accumulated to suggest that an aberration in the signal transduction pathways contributes to the pathophysiology of cardiovascular disease. Several components of the signaling pathways have been identified as potential targets for the development of new therapies of cardiovascular disease. Therefore, this volume has been compiled to highlight the contributions of different signaling systems in modulating normal cardiovascular functions and how a perturbation in these signaling events leads to abnormal cell functions and cardiovascular disorders. This volume has been divided into five sections dealing with five key signaling pathways regulating different aspects of cardiovascular physiology. The first section describes the role of G-protein-coupled receptor (GPCR) signaling in cardiovascular functions. In this section, Anand-Srivastava has elegantly summarized studies showing that the expression levels of various G-proteins as well as responsiveness of adenylyl cyclase systems to various stimuli such as β-adrenergic receptor (βAR) agonist and vasoactive peptides are defective in various models of hypertension, congestive heart failure (CHF), cardiac hypertrophy, and other diseases. Dent et al. have highlighted studies showing how the alterations in different components of the βAR signaling system contribute to CHF and suggest that βAR blockade could be used as a strategy to treat CHF. Continuing on the same theme, Vacek et al. have reviewed the pathophysiological mechanisms involved in CHF and sudden cardiac death, with an emphasis on the role of homocysteine-induced cross talk between NMDA receptor and GPCRs, while Moolman et al. have elaborated on the contributions of adenosine, cAMP/PKA system as well as p 38mapk in eliciting a cardioprotective response during early preconditioning. This section also has two elegant articles on the role of angiotensin II in cardiovascular pathophysiology: Engberding and Grindling and Schaffer and Mozaffari have provided indepth accounts of various signaling pathways induced by angiotensin II and how the dysregulation of this pathway contributes to heightened growth, proliferation, hypertrophy, and cell survival death responses associated with various cardiovascular abnormalities. v vi PrefaceThe second section foc...

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Hypoxia and glucose independently regulate the beta-adrenergic receptor-adenylate cyclase system in cardiac myocytes.

Cited by 32 publications

References 61 publications

A Selective ε-Protein Kinase C Antagonist Inhibits Protection of Cardiac Myocytes from Hypoxia-induced Cell Death

A Selective ε-Protein Kinase C Antagonist Inhibits Protection of Cardiac Myocytes from Hypoxia-induced Cell Death

Regulation of Sympathetic Activity in Children with Various Congenital Heart Diseases

Signal Transduction in the Cardiovascular System in Health and Disease

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