Phenylephrine induces activation of CREB in adult rat cardiac myocytes through MSK1 and PKA signaling pathways

Markou, Thomais; Hadzopoulou-Cladaras, Margarita; Lazou, Antigone

doi:10.1016/j.yjmcc.2004.08.002

Cited by 68 publications

(51 citation statements)

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“…In one study it was found that the b-adrenergic receptor agonist isoproterenol, as well as b-adrenergic receptor antagonists, were not influenced by the expression of ANP mRNA in isolated cardiomyocytes (Ander et al, 2004). Others have found that ANP mRNA expression in adult cardiomyocytes is increased in response to phenylephrine (Markou et al, 2004). Several studies in vitro have shown that catecholamines can enhance the release of ANP from the myocytes by a-adrenergic (Ambler and Leite, 1994;Currie and Newman, 1986;Toth et al, 1986;Wong et al, 1988) as well as b-adrenergic stimulation (Gibbs, 1987;Ruskoaho and Leppaluoto, 1988;Schiebinger et al, 1987).…”

Section: Importance Of the Natriuretic Peptide Receptorsmentioning

confidence: 99%

Receptor binding occurrence and plasma levels of natriuretic peptides in response to sympathectomy

Hansson

2005

Microsc. Res. Tech.

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In the present investigation the relationship between the sympathetic nervous system and the endocardial levels of receptor binding sites for natriuretic peptides and the plasma content of atrial natriuretic peptide were analyzed in rats. In order to destruct the cardiac sympathetic nerve terminals, chemical sympathectomy with 6-hydroxydopamine was made in parallel with intravenous measurements of blood pressure and heart frequency. By use of immunohistochemical and enzyme-linked-immunosorbent techniques the expression of tyrosine hydroxylasepositive sympathetic nerve terminals and plasma levels of pro-atrial natriuretic peptide were determined, respectively. The occurrence of receptor binding sites for natriuretic peptides was examined by in vitro receptor autoradiography. In contrast to the marked occurrence of natriuretic peptide receptor binding sites seen in the ventricular endocardium of control rats, the sympathectomized rats exhibited a decreased number of binding sites for natriuretic peptides in the endocardium of both the right and left chambers. Interestingly, this was found in parallel with a significant decrease of systolic and diastolic blood pressure and increased plasma levels of pro-atrial natriuretic peptide in the treated group of rats. These findings, together with those in previous studies, give support to an idea that one part of the blood pressure-decreasing effects, seen in patients treated with b-adrenergic blockade, might be through a reduction of the natriuretic clearance receptor C, then giving rise to increased levels of atrial natriuretic peptide. Microsc. Res. Tech. 67:90-99, 2005. V

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Section: Importance Of the Natriuretic Peptide Receptorsmentioning

confidence: 99%

Receptor binding occurrence and plasma levels of natriuretic peptides in response to sympathectomy

Hansson

2005

Microsc. Res. Tech.

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“…water and incubated in a 37°C incubator for 7 d to induce aggregation. The aggregated Aβ [25][26][27][28][29][30][31][32][33][34][35] was then diluted to 500 µM and stored at −80°C before use. 22) Cell Viability Assay The MTT assay was carried out as previously described.…”

Section: )mentioning

confidence: 99%

“…After 10 d's culture, neurons were exposed to Aβ [25][26][27][28][29][30][31][32][33][34][35] at different concentrations (10,20,30,40 and 50 µM) for 24 h, then MTT assay was used to determine the cell viability. Results showed that Aβ [25][26][27][28][29][30][31][32][33][34][35] insult decreased cell survival in a concentration dependent manner (Fig. 4A), and 30 µM of Aβ [25][26][27][28][29][30][31][32][33][34][35] was the sublethal level, thus was used in the following experiments.…”

Section: Osthole Reduced Intracellular Aβ Levels In Neural Cellsmentioning

confidence: 99%

“…Our data showed that osthole reduced intracellular Aβ levels in neural cells, which was associated with decreased BACE1 protein; osthole reversed exogenous Aβ 25-35 -induced cell viability loss, apoptosis, and synapsin-1 reduction, which was related to the reestablishment of phosphorylation of cyclic AMP response element-binding protein (CREB). The collective evidence indicates that osthole possesses the ability to protect cortical neurons and SH-SY5Y cells against Aβ injury, and the underlying mechanism may be attributed to the enhancement of CREB phosphorylation.Key words osthole; Alzheimer's disease; cyclic AMP response element-binding protein; β-amyloid peptide [25][26][27][28][29][30][31][32][33][34][35] Alzheimer's disease (AD) is an irreversible neurodegenerative disorder of the brain characterized by progressive cognitive loss and memory decline. The abnormal deposition of β-amyloid peptide (Aβ) is one of the most notable neuropathological hallmarks of AD.…”

mentioning

confidence: 99%

“…Key words osthole; Alzheimer's disease; cyclic AMP response element-binding protein; β-amyloid peptide [25][26][27][28][29][30][31][32][33][34][35] Alzheimer's disease (AD) is an irreversible neurodegenerative disorder of the brain characterized by progressive cognitive loss and memory decline. The abnormal deposition of β-amyloid peptide (Aβ) is one of the most notable neuropathological hallmarks of AD.…”

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Osthole Reverses Beta-Amyloid Peptide Cytotoxicity on Neural Cells by Enhancing Cyclic AMP Response Element-Binding Protein Phosphorylation

Wen

Liang

et al. 2013

Biological & Pharmaceutical Bulletin

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Accumulation of β-amyloid peptide (Aβ) in the brain plays an important role in the pathogenesis of Alzheimer's disease (AD). Previous studies have demonstrated the neuroprotective role of osthole against oxygen and glucose deprivation in cortical neurons. However, the effects of osthole on Aβ-induced neurotoxicity in neural cells have rarely been reported. The current study was designed to investigate the protective effects of osthole on a cell model of AD insulted by exogenous Aβ 25-35 and the potential mechanism(s). In this study, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, immunofluorescence analysis, apoptosis assay, reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) techniques were used in primary cortical neurons and SH-SY5Y cells. Our data showed that osthole reduced intracellular Aβ levels in neural cells, which was associated with decreased BACE1 protein; osthole reversed exogenous Aβ 25-35 -induced cell viability loss, apoptosis, and synapsin-1 reduction, which was related to the reestablishment of phosphorylation of cyclic AMP response element-binding protein (CREB). The collective evidence indicates that osthole possesses the ability to protect cortical neurons and SH-SY5Y cells against Aβ injury, and the underlying mechanism may be attributed to the enhancement of CREB phosphorylation.Key words osthole; Alzheimer's disease; cyclic AMP response element-binding protein; β-amyloid peptide [25][26][27][28][29][30][31][32][33][34][35] Alzheimer's disease (AD) is an irreversible neurodegenerative disorder of the brain characterized by progressive cognitive loss and memory decline. The abnormal deposition of β-amyloid peptide (Aβ) is one of the most notable neuropathological hallmarks of AD. Aβ-Induced synaptic loss and subsequent neuronal death have been implicated as a major cause of the cognitive decline associated with AD.1-4) Accumulating evidence suggests that multiple cellular targets and signaling pathways mediate Aβ-induced neurotoxicity, including N-methyl-D-aspartate (NMDA) receptors and cyclic AMP response element-binding protein (CREB).5,6) CREB is a prosurvival transcription factor responsible for the expression of a large number of downstream genes, 7) such as brain-derived neurotrophic factor (BDNF), an important neurotrophic factor that possessed ability to promote neural protection, plasticity, and regeneration in a variety of conditions, such as central nervous system (CNS) injury, cerebral ischemia, and electrical stimulation.8-10) It is well established that several protein kinase pathways converge to co-regulate CREB activity. Aβ has been shown to interfere with events downstream of activated CREB, especially gene expression of BDNF.11) Moreover, reduced phosphorylation of CREB (p-CREB) has been observed in postmortem brains of AD patients and in transgenic (Tg)-AD mice overexpressing Aβ.12,13) It has been reported that enhanced CREB function in the CA1 region of the dorsal hippocampus rescues the spatia...

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Signalling pathways evoked by α1-adrenoceptors in human melanoma cells

Scarparo

Visconti

Castrucci

2006

Cell Biochem. Funct.

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The biological effects of catecholamines in mammalian pigment cells are poorly understood, but in poikilothermic vertebrates they regulate the translocation of pigment granules. We have previously demonstrated in SK-Mel 23-human melanoma cells the presence of low affinity alpha(1)-adrenoceptors, which mediate a decrease in cell proliferation and increase in tyrosinase activity, with no change of tyrosinase expression. In this report, we investigated the signalling pathways involved in these responses. Calcium mobilization in response to phenylephrine (PHE), an alpha(1)-adrenergic agonist, was investigated by confocal microscopy, and no change of fluorescence during the treatment was observed, suggesting that calcium is not involved in the signalling pathway activated by alpha(1)-adrenoceptors in SK-Mel 23 cells. cAMP levels, determined by enzyme-immunoassay, were significantly increased by PHE (10(-5)-10(-4)M), that could be blocked by the alpha(1)-adrenergic antagonist benoxathian (10(-5)-10(-4)M). Several biological assays were then performed with PHE, for 72 h, in the absence or presence of various signalling pathway inhibitors, in an attempt to determine the intracellular messengers involved in the responses of proliferation and tyrosinase activity. Our results suggest the participation of p38 and ERKs in PHE-induced decrease of proliferation, and possibly also of cAMP and protein kinase A. Regarding PHE-induced increase of tyrosinase activity, it is suggested that the following signalling components are involved: cAMP/PKA, PKC, PI3K, p38 and ERKs.

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Phenylephrine induces activation of CREB in adult rat cardiac myocytes through MSK1 and PKA signaling pathways

Cited by 68 publications

References 35 publications

Receptor binding occurrence and plasma levels of natriuretic peptides in response to sympathectomy

Receptor binding occurrence and plasma levels of natriuretic peptides in response to sympathectomy

Osthole Reverses Beta-Amyloid Peptide Cytotoxicity on Neural Cells by Enhancing Cyclic AMP Response Element-Binding Protein Phosphorylation

Signalling pathways evoked by α1-adrenoceptors in human melanoma cells

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