The effect of substance P on asthmatic rat airway smooth muscle cell proliferation, migration, and cytoplasmic calcium concentration in vitro

Li, Miao; Shang, Yunxiao; Wei, Bing; Yu, Yang

doi:10.1186/1476-9255-8-18

Cited by 25 publications

(14 citation statements)

References 25 publications

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“…ASMCs are important effector cells in asthma [11] . Recently, Sukkar and colleagues have shown that in addition to ASMCs demonstrating the ability to contract, they can transform into a proliferative phenotype when stimulated by external environment factors [1] .…”

Section: Discussionmentioning

confidence: 99%

Effects of mitochondrial ATP-sensitive K+ channel on protein kinase C pathway and airway smooth muscle cell proliferation in asthma

Wan

Zhao

Xie

2012

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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The effects of ATP-sensitive mitochondrial K(+) channel (mitoK(ATP)) on mitochondrial membrane potential (Δψm), cell proliferation and protein kinase C alpha (PKCα) expression in airway smooth muscle cells (ASMCs) were investigated. Thirty-six Sprague-Dawley (SD) rats were immunized with saline (controls) or ovalbumin (OVA) with alum (asthma models). ASMCs were cultured from the lung of control and asthma rats. ASMCs were treated with diazoxide (the potent activator of mitoK(ATP)) or 5-hydroxydencanote (5-HD, the inhibitor of mitoK(ATP)). Rhodamine-123 (R-123) was used to detect Δψm. The expression of PKCα protein was examined by using Western blotting, while PKCα mRNA expression was detected by using real-time PCR. The proliferation of ASMCs was measured by MTT assay and cell cycle analysis. In diazoxide-treated normal ASMCs, the R-123 fluorescence intensity, protein and mRNA levels of PKCα, MTT A values and percentage of cells in S phase were markedly increased as compared with untreated controls. The ratio of G(0)/G(1) cells was decreased (P<0.05) in diazoxide-treated ASMCs from normal rats. However, there were no significant differences between the ASMCs from healthy rats treated with 5-HD and the normal control group. In untreated and diazoxide-treated ASMCs of asthmatic rats, the R-123 fluorescence intensity, protein and mRNA levels of PKCα, MTT A values and the percentage of cells in S phase were increased in comparison to the normal control group. Furthermore, in comparison to ASMCs from asthmatic rats, these values were considerably increased in asthmatic group treated with diazoxide (P<0.05). After exposure to 5-HD for 24 h, these values were decreased as compared with asthma control group (P<0.05). In ASMCs of asthma, the signal transduction pathway of PKCα may be involved in cell proliferation, which is induced by the opening of mitoK(ATP) and the depolarization of Δψm.

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Section: Discussionmentioning

confidence: 99%

Effects of mitochondrial ATP-sensitive K+ channel on protein kinase C pathway and airway smooth muscle cell proliferation in asthma

Wan

Zhao

Xie

2012

J. Huazhong Univ. Sci. Technol. [Med. Sci.]

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“…On the other hand, prolonged dopaminergic signaling via a D2-like, Gi-coupled pathway leads to enhancement of the Gs-coupled ␤2-adrenoceptor (␤2AR) system, thus increasing cAMP and promoting bronchodilation. GRK3, G protein-coupled receptor kinase; RGS4, G-protein signaling 4. dence for TRPV1 in nonneuronal airway cells such as epithelium (298) and ASM (354) but considerable data on the expression of kinin receptors in ASM (173,200,252,322). Thus it would be interesting to determine whether OGR1 can indirectly influence these mechanisms.…”

Section: Asm [Ca 2ϩ ] I and Contractilitymentioning

confidence: 99%

Airway smooth muscle in airway reactivity and remodeling: what have we learned?

Prakash

2013

American Journal of Physiology-Lung Cellular and Molecular Phys

172

154

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Prakash YS. Airway smooth muscle in airway reactivity and remodeling: what have we learned? Am J Physiol Lung Cell Mol Physiol 305: L912-L933, 2013. First published October 18, 2013 doi:10.1152/ajplung.00259.2013.-It is now established that airway smooth muscle (ASM) has roles in determining airway structure and function, well beyond that as the major contractile element. Indeed, changes in ASM function are central to the manifestation of allergic, inflammatory, and fibrotic airway diseases in both children and adults, as well as to airway responses to local and environmental exposures. Emerging evidence points to novel signaling mechanisms within ASM cells of different species that serve to control diverse features, including 1) [Ca 2ϩ ]i contractility and relaxation, 2) cell proliferation and apoptosis, 3) production and modulation of extracellular components, and 4) release of pro-vs. anti-inflammatory mediators and factors that regulate immunity as well as the function of other airway cell types, such as epithelium, fibroblasts, and nerves. These diverse effects of ASM "activity" result in modulation of bronchoconstriction vs. bronchodilation relevant to airway hyperresponsiveness, airway thickening, and fibrosis that influence compliance. This perspective highlights recent discoveries that reveal the central role of ASM in this regard and helps set the stage for future research toward understanding the pathways regulating ASM and, in turn, the influence of ASM on airway structure and function. Such exploration is key to development of novel therapeutic strategies that influence the pathophysiology of diseases such as asthma, chronic obstructive pulmonary disease, and pulmonary fibrosis.

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“…As a family of structurally related neuropeptides, TACs are distributed in the central nervous system and have roles as neurotransmitters and/or neuromodulators (29). Some studies have reported that neurokinins participate in asthmatic airway inflammation, and substance P has a role in asthmatic rat airway smooth muscle cell proliferation, migration and cytoplasmic calcium concentration in vitro (30,31). The previous studies have verified that the mutation of CEP290 cause a number of debilitating and phenotypically distinct human diseases (32).…”

Section: Discussionmentioning

confidence: 97%