Messenger RNA for the guanine nucleotide-binding regulatory protein (G protein) is reduced in the acute ischemic myocardium

Ohyanagi, Mitsumasa; Yamamoto, Juro; Nakamura, Kiyoko; Shibuya, Jun; Morita, Masato; Masutani, Motomaru; Arii, Tohru; Iwasaki, Tadaaki

doi:10.1016/0022-2828(95)90049-7

Cited by 14 publications

(2 citation statements)

References 20 publications

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“…Furthermore, the densities of ADP-ribosylation or antibody binding. Similar results were b -and b -adrenoreceptors were decreased in the isreported by different groups using different animal models 1 2 chemic-reperfused hearts and the isoproterenol-stimulated [107][108][109]. In view of the role of b-adrenoceptor pathway 21 adenylyl cyclase activity was depressed.…”

Section: Antioxidants Protect the Alteration Of B-supporting

confidence: 61%

Status of myocardial antioxidants in ischemia–reperfusion injury

Dhalla

Elmoselhi

Hata

et al. 2000

Cardiovascular Research

703

444

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Background: Myocardial ischemia-reperfusion represents a clinically relevant problem associated with thrombolysis, angioplasty and coronary bypass surgery. Injury of myocardium due to ischemia-reperfusion includes cardiac contractile dysfunction, arrhythmias as well as irreversible myocyte damage. These changes are considered to be the consequence of imbalance between the formation of oxidants and the availability of endogenous antioxidants in the heart. Observations: An increase in the formation of reactive oxygen species during ischemia-reperfusion and the adverse effects of oxyradicals on myocardium have now been well established by both direct and indirect measurements. Although several experimental studies as well as clinical trials have demonstrated the cardioprotective effects of antioxidants, some studies have failed to substantiate the results. Nonetheless, it is becoming evident that some of the endogenous antioxidants such as glutathione peroxidase, superoxide dismutase, and catalase act as a primary defense mechanism whereas the others including vitamin E may play a secondary role for attenuating the ischemia-reperfusion injury. The importance of various endogenous antioxidants in suppressing oxidative stress is evident from the depression in their activities and the inhibition of cardiac alterations which they produce during ischemia-reperfusion injury. The effects of an antioxidant thiol containing compound, N-acetylcysteine, and ischemic preconditioning were shown to be similar in preventing changes in the ischemic-reperfused hearts. Conclusions: The available evidence support the role of oxidative stress in ischemia-reperfusion injury and emphasize the importance of antioxidant mechanisms in cardioprotection.

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Section: Antioxidants Protect the Alteration Of B-supporting

confidence: 61%

Status of myocardial antioxidants in ischemia–reperfusion injury

Dhalla

Elmoselhi

Hata

et al. 2000

Cardiovascular Research

703

444

View full text Add to dashboard Cite

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“…mRNA was reportedly induced or increased for such proteins as ␤-adrenergic receptor kinase 1, which inactivates ␤-receptors (33); ␤ 1adrenergic receptors per se (12); heat shock proteins 70 (16,24,35), 72 (29), and 90 (27), which are most intensely expressed in reperfusion, perhaps as a result of secondary oxidative injury; vascular endothelial growth factor and endothelin-1 (1,9,32); interleukin-6 and intracellular adhesion molecule (15,36); insulinlike growth factor II (13); and the Na ϩ /H ϩ exchanger (4). Other reports have described the appearance of two new heart transcripts and three new stress-inducible genes in response to ischemia (14) and the suppression of mRNA message regulating G s and G i proteins, which may explain the observed disruption to the G proteinadenylate cyclase system (28).…”

mentioning

confidence: 89%

Alteration of gene expression for glycolytic enzymes in aerobic and ischemic myocardium

Liedtke

Lynch

1999

American Journal of Physiology-Heart and Circulatory Physiology

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The purpose of this report was to describe mRNA abundance for the glycolytic enzymes glyceraldehyde-3-phosphate dehydrogenase (GAPDH), pyruvate kinase, and pyruvate dehydrogenase in ischemic and adjacent aerobic myocardium. Mechanical, metabolic, and mRNA data were acquired in a pig model of regulated coronary flow using extracorporeal perfusion. Trials of coronary hypoperfusion included sustained and intermittent exposures of acute ischemia with or without reperfusion. These were compared with a chronic 4-day model of partial coronary stenosis. In ischemic tissues, levels of mRNA, normalized by mRNA for beta-actin, were increased over control values for GAPDH (range 2.7- to 4.6-fold), pyruvate kinase (2.9-fold), and pyruvate dehydrogenase (2.1-fold). It is of interest that increases in mRNA levels over control values were also observed in adjacent aerobic heart muscle from intervention hearts, including 3.6- to 4.5-fold elevations in message for GAPDH and a 2.1-fold increase in signal for pyruvate dehydrogenase. Augmentation in mRNA abundance occurred in as short a time as 40 min of ischemia and was maintained for as long as 4 days in partial coronary stenosis. Whether the former time was of an interval sufficient to affect protein production is problematic, but the latter time was ample to influence enzyme concentration, which may in turn have regulated glycolysis in this condition.

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Implication of G-proteins in Cardiovascular Disease

Anand‐Srivastava

2008

Signal Transduction in the Cardiovascular System in Health and Disease

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Messenger RNA for the guanine nucleotide-binding regulatory protein (G protein) is reduced in the acute ischemic myocardium

Cited by 14 publications

References 20 publications

Status of myocardial antioxidants in ischemia–reperfusion injury

Status of myocardial antioxidants in ischemia–reperfusion injury

Alteration of gene expression for glycolytic enzymes in aerobic and ischemic myocardium

Implication of G-proteins in Cardiovascular Disease

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