Tyrosine kinase-dependent calcium signaling in airway smooth muscle cells

Tolloczko, Barbara; Tao, Florence; Zacour, Mary; Martin, James G.

doi:10.1152/ajplung.2000.278.6.l1138

Cited by 33 publications

(38 citation statements)

References 35 publications

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“…Briefly, agonist-induced depletion of the internal store triggers activation of protein tyrosine kinases (PTK), Ras and reorganisation of the cytoskeleton in such a way as to directly couple IP 3 receptors on the SR with Ca 2+ channels on the plasmalemma. Several observations made in ASM are consistent with such a mechanism: 1) spasmogenic stimulation of ASM is accompanied by activation of PTKs [186,187] and Ras/ Rho [188][189][190][191], as well as cytoskeletal rearrangement [189,191,192]; 2) inhibition of PTK compromises SR refilling [193]; 3) ASM depleted of FAK, which regulates cytoskeleton stability, shows marked suppression of cholinergic Ca 2+ transients and contractions as well as changes in voltagedependent Ca 2+ channel function, without any disruptive changes in the contractile apparatus per se when assessed by addition of Ca 2+ to permeabilised muscle strips [194]; 4) in the rat ASM, RyR1 on the SR co-localise with voltage-dependent Ca 2+ channels on the plasmalemma [27]. However, the possible role for this novel SR refilling pathway has not yet been tested in ASM: the use of inhibitors of cytoskeletal organisation (e.g.…”

Section: +supporting

confidence: 61%

Ionic mechanisms and Ca2+ handling in airway smooth muscle

Hirota

Helli²,

Janssen³

2007

European Respiratory Journal

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Asthma is a disease characterised by reversible contraction of airway smooth muscle. Many signalling pathways are now known to underlie that contraction, almost all of which revolve around Ca 2+ handling. Ca 2+ homeostasis in turn is governed by a wide variety of ionic mechanisms, which are still poorly understood. The present review will briefly summarise those mechanisms that have been recognised for decades, but will then devote considerable attention to several novel ionic signalling mechanisms such as capacitative Ca 2+ entry, the reverse mode of

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Section: +supporting

confidence: 61%

Ionic mechanisms and Ca2+ handling in airway smooth muscle

Hirota

Helli²,

Janssen³

2007

European Respiratory Journal

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“…Rat tracheas were dissected and excess connective tissue was removed [35]. Tissues were digested in elastase at 37uC for 30 min and subsequently placed on ice to stop the reaction.…”

Section: Effects Of Ltd 4 Egf and Hb-egf On Proliferation Of Primarmentioning

confidence: 99%

“…Cell culture reagents were purchased from GIBCO (Invitrogen). The phenotype was confirmed as previously described [35]. Cells at passages 2-4 were used for the experiment.…”

Section: Effects Of Ltd 4 Egf and Hb-egf On Proliferation Of Primarmentioning

confidence: 99%

The epidermal growth factor receptor mediates allergic airway remodelling in the rat

Tamaoka¹,

Hassan²,

McGovern³

et al. 2008

European Respiratory Journal

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The chronicity of bronchial asthma is attributed to persistent airway inflammation and to a variety of structural changes, or remodelling, that includes smooth muscle and goblet cell hyperplasia.To investigate the mechanisms of airway remodelling, the current authors used an established allergen (ovalbumin; OVA)-driven rodent model (the Brown Norway rat).Brown Norway rats were sensitised to OVA and challenged three times at 5-day intervals to evoke airway remodelling. The effects of an epidermal growth factor (EGF) receptor inhibitor, AG1478, and a cysteinyl leukotriene-1 receptor antagonist, montelukast, on epithelial and airway smooth muscle (ASM) cell proliferation in vivo in response to repeated OVA challenge were tested. Three challenges with leukotriene (LT)D 4 were given, to examine their effects on remodelling with and without AG1478 pretreatment.OVA challenges caused ASM hyperplasia, with an increase in mass, epithelial cell proliferation and goblet cell proliferation. AG1478 prevented the changes, as did montelukast. Multiple OVA challenges increased heparin-binding EGF-like growth factor but not EGF expression by airway epithelium. LTD 4 reproduced the changes in remodelling induced by OVA and this was blocked by AG1478.Allergen-induced airway epithelial and airway smooth muscle remodelling is mediated by cysteinyl leukotrienes via the cysteinyl leukotriene-1 receptor with downstream effects on the epidermal growth factor receptor axis.KEYWORDS: Allergy, inflammation, lung, signal transduction A sthmatic airways often show extensive and complex remodelling [1][2][3][4]. The growth of smooth muscle has the potential to have the most significant pathophysiological consequences through excessive airway narrowing and airway hyperresponsiveness [5,6]. Increase in airway smooth muscle (ASM) in the airways has been associated with the severity of asthma [3,7], and when present in excess in the large airways is associated with mortality [8]. It is known that hyperplasia of smooth muscle in animal models [9][10][11] and both hyperplasia and hypertrophy in airway specimens from human subjects [12,13] contribute to the increase in ASM mass. It has also been proposed that migration of subepithelial myofibroblasts may add to the tissue mass [7].The mechanism of the growth response of muscle is quite uncertain, although several descriptive studies of growth factor expression in human airway tissues have been reported [14][15][16] and many growth factors have been demonstrated to have mitogenic effects on ASM in culture [17][18][19][20]. Cysteinyl (cys)-leukotrienes (LTs) are known to be involved in allergen-induced ASM cell proliferation in vivo [21,22] but in vitro these substances are weak mitogens for ASM [23,24]. In the sensitised mouse, cys-LT 1 receptor (cys-LT 1 R) antagonism prevents an increase in ASM thickening after repeated allergen challenge [25,26]. It is possible that the effects of cys-LTs in vivo are indirect and mediated by altering the expression of or potentiating the effects of tyrosi...

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“…For the measurement of calcium, cells were loaded with the Ca 2ϩ -sensitive dye, fura 2-AM (Molecular Probes) according to the previously described methods (18) and imaged using an intensified charge-coupled device camera (IC200) and PTI software at a single emission wavelength (510 nm) with a double excitatory wavelength (340 and 380 nm). Fluorescence ratio (340/380) was measured in cells stimulated with CCL3 or CCL23 (1, 10, and 100 ng/ml) or appropriate vehicle.…”

Section: Measurement Of Intracellular Free Ca 2ϩmentioning

confidence: 99%

Expression and Regulation of CCR1 by Airway Smooth Muscle Cells in Asthma

Joubert

Lajoie-Kadoch

Welman

et al. 2008

The Journal of Immunology

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C-C chemokines such as CCL11, CCL5, and CCL3 are central mediators in the pathogenesis of asthma. They are mainly associated with the recruitment and the activation of specific inflammatory cells, such as eosinophils, lymphocytes, and neutrophils. It has recently been shown that they can also activate structural cells, such as airway smooth muscle and epithelial cells. The aims of this study were to examine the expression of the CCL3 receptor, CCR1, on human airway smooth muscle cells (ASMC) and to document the regulation of this receptor by cytokines involved in asthma pathogenesis. We first demonstrated that CCR1 mRNA is increased in the airways of asthmatic vs control subjects and showed for the first time that ASMC express CCR1 mRNA and protein, both in vitro and in vivo. Calcium mobilization by CCR1 ligands confirmed its functionality on ASMC. Stimulation of ASMC with TNF-α and, to a lesser extent, IFN-γ resulted in an up-regulation of CCR1 expression, which was totally suppressed by both dexamethasone or mithramycin. Taken together, our data suggest that CCR1 might be involved in the pathogenesis of asthma, through the activation of ASMC by its ligands.

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Tyrosine kinase-dependent calcium signaling in airway smooth muscle cells

Cited by 33 publications

References 35 publications

Ionic mechanisms and Ca2+ handling in airway smooth muscle

Ionic mechanisms and Ca2+ handling in airway smooth muscle

The epidermal growth factor receptor mediates allergic airway remodelling in the rat

Expression and Regulation of CCR1 by Airway Smooth Muscle Cells in Asthma

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