scholarly journals Ligand-independent Activation of the Glucocorticoid Receptor by β2-Adrenergic Receptor Agonists in Primary Human Lung Fibroblasts and Vascular Smooth Muscle Cells

1999 ◽  
Vol 274 (2) ◽  
pp. 1005-1010 ◽  
Author(s):  
Oliver Eickelberg ◽  
Michael Roth ◽  
Rainer Lörx ◽  
Victoria Bruce ◽  
Jochen Rüdiger ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Glucocorticoid Receptor ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Adrenergic Receptor ◽  
Human Lung ◽  
Lung Fibroblasts ◽  
Human Lung Fibroblasts ◽  
Β2 Adrenergic Receptor

scholarly journals Inhibitory effect of D1-like and D3 dopamine receptors on norepinephrine-induced proliferation in vascular smooth muscle cells

2008 ◽  
Vol 294 (6) ◽  
pp. H2761-H2768 ◽  
Author(s):  
Zhen Li ◽  
Changqing Yu ◽  
Yu Han ◽  
Hongmei Ren ◽  
Weibin Shi ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Protein Kinase ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Adrenergic Receptor ◽  
Receptor Agonist ◽  
Thymidine Incorporation ◽  
Inhibitory Effect ◽  
Vsmc Proliferation

The sympathetic nervous system plays an important role in the regulation of blood pressure. There is increasing evidence for positive and negative interactions between dopamine and adrenergic receptors; the activation of the α-adrenergic receptor induces vasoconstriction, whereas the activation of dopamine receptor induces vasorelaxation. We hypothesize that the D1-like receptor and/or D3 receptor also inhibit α1-adrenergic receptor-mediated proliferation in vascular smooth muscle cells (VSMCs). In this study, VSMC proliferation was determined by measuring [3H]thymidine incorporation, cell number, and uptake of 3-(4,5-dimethylthiazol-2-yl)-diphenyltetrazolium bromide (MTT). Norepinephrine increased VSMC number and MTT uptake, as well as [3H]thymidine incorporation via the α1-adrenergic receptor in aortic VSMCs from Sprague-Dawley rats. The proliferative effects of norepinephrine were attenuated by the activation of D1-like receptors or D3 receptors, although a D1-like receptor agonist, fenoldopam, and a D3 receptor agonist, PD-128907, by themselves, at low concentrations, had no effect on VSMC proliferation. Simultaneous stimulation of both D1-like and D3 receptors had an additive inhibitory effect. The inhibitory effect of D3 receptor was via protein kinase A, whereas the D1-like receptor effect was via protein kinase C-ζ. The interaction between α1-adrenergic and dopamine receptors, especially D1-like and D3 receptors in VSMCs, could be involved in the pathogenesis of hypertension.

Ubiquitous expression of phosphodiesterase 7A in human proinflammatory and immune cells

2003 ◽  
Vol 284 (2) ◽  
pp. L279-L289 ◽  
Author(s):  
Susan J. Smith ◽  
Steven Brookes-Fazakerley ◽  
Louise E. Donnelly ◽  
Peter J. Barnes ◽  
Mary S. Barnette ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
T Cell ◽  
T Lymphocytes ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cardiac Myocytes ◽  
Cell Lines ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Lung Fibroblasts

We have determined the expression of phosphodiesterase (PDE) 7A1 and PDE7A2 in human cells that have been implicated in the pathogenesis of chronic obstructive pulmonary disease and asthma. Messenger RNA transcripts were detected by RT-PCR in T lymphocytes, monocytes, neutrophils, airway and vascular smooth muscle cells, lung fibroblasts, epithelial cells, and cardiac myocytes. Human epithelial, T cell, eosinophil, and lung fibroblast cell lines were also positive for PDE7A1 and PDE7A2 mRNA transcripts. By Western immunoblot analyses the amount of PDE7A1 was greatest in T cell lines, peripheral blood T lymphocytes, epithelial cell lines, airway and vascular smooth muscle cells, lung fibroblasts, and eosinophils but was not detected in neutrophils. In contrast, PDE7A2 protein, which was identified in human cardiac myocytes, was not found in any of the other cell types investigated. Immunoconfocal analyses showed that PDE7A was expressed in neutrophils and alveolar macrophages. As the expression of PDE7A mirrors the distribution of PDE4 we speculate that this enzyme could be a target for novel anti-inflammatory drugs.

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