Regulation of histamine H<sub>1</sub> receptor coupling by dexamethasone in human cultured airway smooth muscle

Hardy, E; Farahani, Mosavar; Hall, Ian P.

doi:10.1111/j.1476-5381.1996.tb15509.x

Cited by 37 publications

(21 citation statements)

References 25 publications

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“…TNFα increases the amount, as well as the activity, of G proteins in several cell types including airway smooth muscle 1719-21 The finding that TNFα enhances calcium mobilisation in response to NaF,7 an agent that bypasses membrane receptors and directly activates G proteins,22 23 supports the notion that TNFα acts directly at the level of G proteins rather than modifying the expression of contractile agonist receptors. This observation supports previous findings that, despite increased calcium signals to carbachol, TNFα did not increase muscarinic receptor numbers 5…”

Section: Potential Intracellular Mechanisms Altered By Cytokinesmentioning

confidence: 85%

Cytokines induce airway smooth muscle cell hyperresponsiveness to contractile agonists

Amrani

Panettieri

1998

Thorax

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Section: Potential Intracellular Mechanisms Altered By Cytokinesmentioning

confidence: 85%

Cytokines induce airway smooth muscle cell hyperresponsiveness to contractile agonists

Amrani

Panettieri

1998

Thorax

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“…There are four subtypes of surface receptors that mediate responses to histamine (H 1 , H 2 , H 3 , and H 4 receptors). Stimulation with histamine is known to increase hydrolysis of phosphoinositol, enhance accumulation of inositol phosphates, and elevate [Ca 2ϩ ] cyt (22). In the human pulmonary vasculature, histamine exerts dual functional effects, both vasoconstrictive and vasodilatory, mediated by receptors located on both PASMC and PAEC (4).…”

Section: Discussionmentioning

confidence: 99%

Histamine-mediated increases in cytosolic [Ca²⁺] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells

Mauban¹,

Wilkinson²,

Schach³

et al. 2006

American Journal of Physiology-Cell Physiology

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Agonist stimulation of human pulmonary artery smooth muscle cells (PASMC) and endothelial cells (PAEC) with histamine showed similar spatiotemporal patterns of Ca(2+) release. Both sustained elevation and oscillatory patterns of changes in cytosolic Ca(2+) concentration ([Ca(2+)](cyt)) were observed in the absence of extracellular Ca(2+). Capacitative Ca(2+) entry (CCE) was induced in PASMC and PAEC by passive depletion of intracellular Ca(2+) stores with 10 microM cyclopiazonic acid (CPA; 15-30 min). The pyrazole derivative BTP2 inhibited CPA-activated Ca(2+) influx, suggesting that depletion of CPA-sensitive internal stores is sufficient to induce CCE in both PASMC and PAEC. The recourse of histamine-mediated Ca(2+) release was examined after exposure of cells to CPA, thapsigargin, caffeine, ryanodine, FCCP, or bafilomycin. In PASMC bathed in Ca(2+)-free solution, treatment with CPA almost abolished histamine-induced rises in [Ca(2+)](cyt). In PAEC bathed in Ca(2+)-free solution, however, treatment with CPA eliminated histamine-induced sustained and oscillatory rises in [Ca(2+)](cyt) but did not affect initial transient increase in [Ca(2+)](cyt). Furthermore, treatment of PAEC with a combination of CPA (or thapsigargin) and caffeine (and ryanodine), FCCP, or bafilomycin did not abolish histamine-induced transient [Ca(2+)](cyt) increases. These observations indicate that 1) depletion of CPA-sensitive stores is sufficient to cause CCE in both PASMC and PAEC; 2) induction of CCE in PAEC does not require depletion of all internal Ca(2+) stores; 3) the histamine-releasable internal stores in PASMC are mainly CPA-sensitive stores; 4) PAEC, in addition to a CPA-sensitive functional pool, contain other stores insensitive to CPA, thapsigargin, caffeine, ryanodine, FCCP, and bafilomycin; and 5) although the CPA-insensitive stores in PAEC may not contribute to CCE, they contribute to histamine-mediated Ca(2+) release.

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“…Conversely, glucocorticoids inhibit expression of NK2 receptors in bovine ASM [94], inhibit m2 mAChR expression in the airway [200], and inhibit the IL-1β-mediated up-regulation of B2 bradykinin (BK) receptors in the airway [201]. Pretreatment of human ASM cells with glucocorticoids significantly inhibits histamine-stimulated phosphoinositide production [202]. Thus the sum of effects of glucocorticoids on GPCR signal transduction components tends to render ASM less responsive to procontractile stimuli and more responsiveness to betaagonists.…”

Section: Altered Gpcr Responsiveness With Therapymentioning

confidence: 99%

Signaling and regulation of G protein-coupled receptors in airway smooth muscle

2003

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Signaling through G protein-coupled receptors (GPCRs) mediates numerous airway smooth muscle (ASM) functions including contraction, growth, and "synthetic" functions that orchestrate airway inflammation and promote remodeling of airway architecture. In this review we provide a comprehensive overview of the GPCRs that have been identified in ASM cells, and discuss the extent to which signaling via these GPCRs has been characterized and linked to distinct ASM functions. In addition, we examine the role of GPCR signaling and its regulation in asthma and asthma treatment, and suggest an integrative model whereby an imbalance of GPCR-derived signals in ASM cells contributes to the asthmatic state.

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Regulation of histamine H₁ receptor coupling by dexamethasone in human cultured airway smooth muscle

Cited by 37 publications

References 25 publications

Cytokines induce airway smooth muscle cell hyperresponsiveness to contractile agonists

Cytokines induce airway smooth muscle cell hyperresponsiveness to contractile agonists

Histamine-mediated increases in cytosolic [Ca²⁺] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells

Signaling and regulation of G protein-coupled receptors in airway smooth muscle

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Regulation of histamine H1 receptor coupling by dexamethasone in human cultured airway smooth muscle

Cited by 37 publications

References 25 publications

Cytokines induce airway smooth muscle cell hyperresponsiveness to contractile agonists

Cytokines induce airway smooth muscle cell hyperresponsiveness to contractile agonists

Histamine-mediated increases in cytosolic [Ca2+] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells

Signaling and regulation of G protein-coupled receptors in airway smooth muscle

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Regulation of histamine H₁ receptor coupling by dexamethasone in human cultured airway smooth muscle

Histamine-mediated increases in cytosolic [Ca²⁺] involve different mechanisms in human pulmonary artery smooth muscle and endothelial cells