The effect of acute ethanol (EtOH) exposure on protein kinase C (PKC) activity in anterior pituitary

Steiner, J.; Kirsteins, L.; LaPaglia, Nancy; Lawrence, A. M.; Williams, Darren W.; Emanuele, N. V.; Emanuele, Mary Ann

doi:10.1016/s0741-8329(96)00113-9

Cited by 19 publications

(13 citation statements)

References 21 publications

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“…Acute ethanol administration to rats induces translocation of the conventional PKCs from the cytosol to Golgi membranes (Stubbs and Slater, 1999). In contrast, ethanol inhibits PKC translocation from the cytosol to membranes in cerebellar granule and anterior pituitary cells (Steiner et al, 1997). Ethanol administration for 5 days decreases PKC␣ and ␥ expression in rat frontal cortex (Narita et al, 2001), whereas ethanol administration for 14 days does not alter PKC␥ expression in cerebral cortex (Kumar et al, 2002).…”

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confidence: 93%

Differential Effects of Systemic Ethanol Administration on Protein Kinase Cϵ, γ, and β Isoform Expression, Membrane Translocation, and Target Phosphorylation: Reversal by Chronic Ethanol Exposure

Kumar

Lane

Morrow

2006

J Pharmacol Exp Ther

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Systemic ethanol administration alters protein kinase C (PKC) activity in brain, but the effects of ethanol on the expression and translocation of specific isoforms are unknown. Rats were administered ethanol (2 g/kg i.p.) or saline and PKC levels were measured in the cytosolic and membrane fractions by Western blot analysis. PKC expression was increased in the cytosol and decreased in the membrane (P2) fraction of cerebral cortex at 10 min. At 60 min, expression of PKC in the P2 fraction was increased by 42.2 Ϯ 12%, but cytosolic levels were unchanged. In contrast, PKC␥ in the P2 fraction was decreased 32.7 Ϯ 7% at 60 min but not at 10 min post-ethanol administration. PKC␥ levels in the cytosol were reduced at 10 min post-ethanol administration and unchanged at 60 min. PKC␤ expression was increased 36 Ϯ 10 and 144 Ϯ 52% in the P2 fraction both at 10 and 60 min post-ethanol administration, whereas cytosolic levels were unchanged. Serine phosphorylation of GABA A receptor ␤-chain was reduced, and phosphorylation of N-methyl-Daspartate receptor NR1 subunit was increased 60 min following ethanol administration. There was no effect of acute ethanol administration on PKC isoform levels in the hippocampus. Ethanol challenge did not alter PKC isoform expression in the P2 fraction of cerebral cortex following chronic ethanol administration. These findings suggest that acute ethanol administration alters PKC synthesis and translocation in an isoform and brain region specific manner that leads to alterations in serine phosphorylation of receptors. Furthermore, chronic ethanol administration prevents ethanol-induced alterations in PKC expression in the P2 fraction, where PKC interacts with ethanolresponsive ion channels.

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confidence: 93%

Differential Effects of Systemic Ethanol Administration on Protein Kinase Cϵ, γ, and β Isoform Expression, Membrane Translocation, and Target Phosphorylation: Reversal by Chronic Ethanol Exposure

Kumar

Lane

Morrow

2006

J Pharmacol Exp Ther

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“…A CUTE ETHANOL NEUROTOXICITY causes reversible alterations in neurotransmission and second messenger signaling (Gordon et al, 1986;Steiner et al, 1997), whereas chronic ethanol neurotoxicity results in permanent loss of function due to structural injury (Bauer and Altman, 1977;Cragg and Phillips, 1985;Gordon et al, 1986;Harper, 1998). In the mature brain, chronic ethanol exposure causes cerebral atrophy, reduced white matter volume, ventricular enlargement, and cerebellar atrophy with loss of Purkinje and granule cell neurons (Bauer and Altman, 1977;Cragg and Phillips, 1985;de la Monte, 1988;Harper, 1998).…”

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confidence: 99%

Partial Rescue of Ethanol‐Induced Neuronal Apoptosis by Growth Factor Activation of Phosphoinositol‐3‐Kinase

Monte

Ganju

Banerjee

et al. 2000

Alcoholism Clin & Exp Res

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“…Because ethanol has been shown to modulate the activities of intracellular signaling pathways in many types of cells (Charness et al, 1996;Deitrich et al, 1996;DePetrillo and Liou, 1993;Diamond and Gordon, 1997;Steiner et al, 1997), it is possible that ethanol also can modulate the intracellular signaling pathway of RBCs that regulates membrane properties related to the deformability. We tested this possibility at concentrations of ethanol that are easily achievable in the blood after alcohol consumption.…”

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confidence: 99%

Ethanol Improves Decreased Filterability of Human Red Blood Cells Through Modulation of Intracellular Signaling Pathways

Oonishi

Sakashita

2000

Alcoholism Clin & Exp Res

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The effect of acute ethanol (EtOH) exposure on protein kinase C (PKC) activity in anterior pituitary

Cited by 19 publications

References 21 publications

Differential Effects of Systemic Ethanol Administration on Protein Kinase Cϵ, γ, and β Isoform Expression, Membrane Translocation, and Target Phosphorylation: Reversal by Chronic Ethanol Exposure

Differential Effects of Systemic Ethanol Administration on Protein Kinase Cϵ, γ, and β Isoform Expression, Membrane Translocation, and Target Phosphorylation: Reversal by Chronic Ethanol Exposure

Partial Rescue of Ethanol‐Induced Neuronal Apoptosis by Growth Factor Activation of Phosphoinositol‐3‐Kinase

Ethanol Improves Decreased Filterability of Human Red Blood Cells Through Modulation of Intracellular Signaling Pathways

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