Subclassification of beta-adrenergic receptors in cultured rat cardiac myoblasts and fibroblasts.

Lau, Yat Hong; Robinson, Remya; Rosen, M R; Bilezikian, J P

doi:10.1161/01.res.47.1.41

Cited by 75 publications

(33 citation statements)

References 26 publications

(22 reference statements)

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“…A 1-g sample of the left and right ventricle was collected for cardiomyocyte dissociation. Heart tissue was minced thoroughly in PBS followed by cellular dissociation with three successive 0.05% trypsin in PBS washes for 20 min at 37°C, adapted from Lau et al (29). Following incubation, the solution was strained through cheesecloth, and cell pellets were collected by spinning at 500 g for 2 min.…”

Section: Methodsmentioning

confidence: 99%

Melatonin supplementation alters uteroplacental hemodynamics and fetal development in an ovine model of intrauterine growth restriction

Lemley

Meyer

Camacho

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

111

109

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Section: Methodsmentioning

confidence: 99%

Melatonin supplementation alters uteroplacental hemodynamics and fetal development in an ovine model of intrauterine growth restriction

Lemley

Meyer

Camacho

et al. 2012

American Journal of Physiology-Regulatory, Integrative and Comp

111

109

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“…Cell Culture-Cardiomyocytes were isolated from the hearts of 2-day-old Wistar rats by a trypsin dispersion procedure using a differential attachment procedure to enrich for cardiomyocytes followed by irradiation as detailed in previous publications (10,11). The final yield of cells was typically 2.5-3 ϫ 10 6 per neonatal heart.…”

Section: Methodsmentioning

confidence: 99%

Protein Kinase D Links Gq-coupled Receptors to cAMP Response Element-binding Protein (CREB)-Ser133 Phosphorylation in the Heart

Özgen

Obreztchikova

Guo

et al. 2008

Journal of Biological Chemistry

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Extracellular ligands stimulate cardiac growth and differentiation by activating a network of protein kinases that phosphorylate transcription factors and alter gene expression. Many of these mechanisms are resurrected in the damaged or failing heart in an attempt to compensate for contractile dysfunction. Our previous studies focused on the cellular actions of thrombin, a serine protease that is generated at sites of cardiac injury and proteolytically activates protease-activated receptor-1 (PAR-1), 3 a G protein-coupled receptor that activates a spectrum of effectors that contribute to cardiac fibroblast proliferation and cardiomyocyte hypertrophy (1). Certain aspects of PAR-1 signaling are cell-specific; PAR-1 activates ERK primarily via an epidermal growth factor receptor (EGFR) transactivation pathway in cardiac fibroblasts and a distinct pathway that does not require EGFR kinase activity in cardiomyocytes. Of note, the PAR-1 signaling pathway in cardiomyocytes triggers a form of cellular remodeling that resembles the changes observed in dilated cardiomyopathies (with pronounced cell elongation and relatively little increased cell width). This hypertrophic phenotype is morphologically distinct from the concentric hypertrophy induced by ␣ 1 -AR agonists such as norepinephrine (NE) or P. multocida toxin (PMT, a direct G␣ q agonist); NE and PMT induce very pronounced increases in overall cell size in association with enhanced sarcomeric organization and atrial natriuretic factor expression (2). cAMP response element-binding protein (CREB) is a bZip transcription factor that forms homo-or heterodimers with itself or with other CREB/ATF family members and binds to specific DNA elements (termed cAMP response elements or CREs) within the regulatory regions of CREB target genes. CREB has been implicated in the maintenance of normal ventricular structure and function; cardiac-specific overexpression of dominant-negative CREB leads to dilated cardiomyopathy and interstitial fibrosis (3). CREB also has been implicated in the electrophysiological remodeling that accompanies pacinginduced cardiac memory in dogs (4). CREB is regulated via phosphorylation at Ser 133 , which activates CREB-dependent gene transcription by recruiting a coactivator (CREB-binding protein, or CBP) to the promoters of CREB target genes.* This work was supported, in whole or in part, by National Institutes of Health Grants HL77860, HL-67101, and HL-28958. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

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“…Neither can it distinguish between receptors that are functionally involved in the production of the tissue response of interest and those that mediate other responses. For instance, rat cardiomyocytes contain only P,-receptors, whereas the P2-receptors occur on non-myocyte cell types (Lau et al, 1980;Buxton & Brunton, 1985;Juberg et al, 1985) (Tsujimoto & Hoffman, 1985). Another difficulty associated with binding studies arises in tissues having a large number of spare receptors; it is known that both cardiac and vascular tissues possess sizeable preceptor reserves that provide for maximal changes in force development when only a small fraction of receptors are occupied by agonists with high intrinsic efficacies (such as isoprenaline) (Venter, 1979;Cohen et al, 1982;Hayes et al, 1984).…”

Section: P2-adrenoceptor-mediated Vascular Responsesmentioning

confidence: 99%

Effects of chronic intravenous infusions of dopexamine and isoprenaline to rats on D₁‐, β₁‐ and β₂‐receptor‐mediated responses

Martin

Broadley

1994

British J Pharmacology

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1 Rats received intravenous infusions of dopexamine, an agonist with selectivity for D1-dopamine receptors and P2-adrenoceptors (240 ,g kg-' h-1), isoprenaline, a P,-and P2-adrenoceptor agonist (40 fig kg- and paced left atrium (increase in tension) showed significant reductions in sensitivity to isoprenaline following isoprenaline infusion. The EC5 values were significantly increased from 5.6 to 17.7 nM in right atria and from 7.4 to 27.1 nM in left atria. The maximum rate increase of right atria was also significantly less after isoprenaline infusion compared with controls (164.0 and 251.9 beats min-', respectively) but the maximum tension responses of left atria were not significantly different. After infusion with dopexamine, however, there was no change in sensitivity of the left or right atria to PI-adrenoceptor stimulation by isoprenaline.3 P2-Adrenoceptor-mediated relaxation responses to isoprenaline of the pulmonary artery, constricted with noradrenaline (6 x 108 M), showed no significant difference in maximum response or ECm in tissue from isoprenaline-or dopexamine-infused rats compared with vehicle-infused controls. P2-Adrenoceptormediated vasodilator responses were also examined in the kidney perfused with the thromboxane A2 analogue, U46619 (7.1 x 10-8 M) to raise perfusion pressure. As with the pulmonary artery, there was no significant difference in ED50 or maximum response to isoprenaline in kidneys from isoprenalineinfused animals compared with vehicle controls.4 The DI-receptor-mediated vasodilator responses to dopamine of the kidney perfused with U46619 were reduced after infusion of rats with dopexamine. The maximum fall in perfusion pressure (16.0 mmHg) and ED50 value (5.2 rig) were significantly different from those after vehicle infusion (31.5 mmHg; 1.5 pg). 5 These results show that functional responses mediated via P1-adrenoceptors and DI-receptors are reduced by intravenous infusions of isoprenaline and dopexamine, respectively. In contrast, the P2-adrenoceptor-mediated vasodilator responses of the pulmonary artery and kidney are not reduced by these agonists. Thus, under identical conditions, there appears to be selective down-regulation of peripheral P,-and D,-receptors, but not of P2-adrenoceptors.

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Subclassification of beta-adrenergic receptors in cultured rat cardiac myoblasts and fibroblasts.

Cited by 75 publications

References 26 publications

Melatonin supplementation alters uteroplacental hemodynamics and fetal development in an ovine model of intrauterine growth restriction

Melatonin supplementation alters uteroplacental hemodynamics and fetal development in an ovine model of intrauterine growth restriction

Protein Kinase D Links Gq-coupled Receptors to cAMP Response Element-binding Protein (CREB)-Ser133 Phosphorylation in the Heart

Effects of chronic intravenous infusions of dopexamine and isoprenaline to rats on D₁‐, β₁‐ and β₂‐receptor‐mediated responses

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Subclassification of beta-adrenergic receptors in cultured rat cardiac myoblasts and fibroblasts.

Cited by 75 publications

References 26 publications

Melatonin supplementation alters uteroplacental hemodynamics and fetal development in an ovine model of intrauterine growth restriction

Melatonin supplementation alters uteroplacental hemodynamics and fetal development in an ovine model of intrauterine growth restriction

Protein Kinase D Links Gq-coupled Receptors to cAMP Response Element-binding Protein (CREB)-Ser133 Phosphorylation in the Heart

Effects of chronic intravenous infusions of dopexamine and isoprenaline to rats on D1‐, β1‐ and β2‐receptor‐mediated responses

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Effects of chronic intravenous infusions of dopexamine and isoprenaline to rats on D₁‐, β₁‐ and β₂‐receptor‐mediated responses