Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.13 (protein kinase C)
 49,245 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Langendorff rat hearts were used (i) to examine whether fentanyl reduces stunning, infarction or both, and (ii) to investigate if this protection is mediated by delta-opioid receptors and/or protein kinase C (PKC). In the stunning study, hearts were subjected to global ischaemia (20 min) and reperfusion. This did not produce infarction. Postischaemic mechanical function was measured in hearts treated with or without fentanyl (740 nM). Fentanyl did not affect postischaemic mechanical function. In the infarction study, the left anterior descending coronary artery was occluded for 35 min and infarct size was assessed by triphenyltetrazolium chloride staining. Hearts in the control group exhibited an infarct zone/area at risk (I/R) of 39 (SEM 5)%, whereas the I/R for the fentanyl group was 13 (2)%. When the hearts were treated with a delta-opioid receptor antagonist (naltrindole 1 nM) or a PKC inhibitor (chelerythrine 2 microM), the effect of fentanyl was abolished, with I/R of 37 (1) and 36 (2)% respectively. In our model, we conclude that fentanyl protects against infarction but not against stunning, and that the limitation of ischaemic injury is mediated by both delta-opioid receptors and PKC.
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PMID:Fentanyl reduces infarction but not stunning via delta-opioid receptors and protein kinase C in rats. 1084 38

The effects of intravenous anesthetics on myocytes have not been fully elucidated. To investigate the effects of various intravenous anesthetics such as fentanyl, morphine, ketamine, diazepam, midazolam, thiamylal, and thiopental on the beta-adrenergic signaling pathway, we measured isoproterenol-stimulated cyclic adenosine monophosphate (cAMP) production in freshly isolated rat ventricular myocytes. Fentanyl, morphine, ketamine, diazepam, and midazolam did not significantly affect isoproterenol-stimulated cAMP production. However, thiamylal and thiopental dose-dependently decreased cAMP production stimulated by isoproterenol or by forskolin, a direct adenylyl cyclase stimulator. In addition, we examined the role of protein kinase C (PKC) as a potential mediator of the thiamylal- or thiopental-induced effects on cAMP production using bisindolylmaleimide I, a non-specific PKC inhibitor. Bisindolylmaleimide I did not alter the inhibitory effects of thiamylal or thiopental. Thiamylal and thiopental significantly decreased isoproterenol-stimulated cAMP production by suppressing the adenylyl cyclase. We conclude that barbiturates such as thiamylal and thiopental decrease isoproterenol-stimulated cAMP production by suppressing the adenylyl cyclase through PKC-independent mechanisms.
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PMID:Thiamylal and thiopental attenuate beta-adrenergic signaling pathway by suppressing adenylyl cyclase in rat ventricular myocytes. 1940 May 52

Mu-opioid receptor regulates microRNA-190 (miR-190) in an agonist-dependent manner; fentanyl, but not morphine, decreases the miR-190 level in rat primary hippocampal neuron cultures and in mouse hippocampi. In this study, the correlation between the cellular content of miR-190 and the mRNA level of its host gene, talin2, suggested that fentanyl decreases the miR-190 level by inhibiting the transcription of talin2. Fentanyl-induced beta-arrestin2-mediated ERK phosphorylation led to the phosphorylation of Yin Yang 1 (YY1). In addition, YY1 phosphorylation impaired the association of YY1 with the -208 to -200 region on the Talin2 promoter, and this association was essential for YY1 to stimulate the transcription of talin2. Thus, fentanyl decreased the transcription of talin2 and subsequently the cellular level of miR-190 by inducing YY1 phosphorylation. In contrast, because morphine induces ERK phosphorylation via the protein kinase C pathway, morphine did not induce YY1 phosphorylation and had no effect on the transcription of talin2 and the cellular content of miR-190. This study therefore delineates a signaling pathway that mediates the effects of fentanyl on miR-190 expression.
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PMID:Yin Yang 1 phosphorylation contributes to the differential effects of mu-opioid receptor agonists on microRNA-190 expression. 2045 14