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Tracheal Smooth Muscle Cells (tracheal + smooth_muscle_cell)

Distribution by Scientific Domains
Life Sciences80%

Kinds of Tracheal Smooth Muscle Cells

  • human tracheal smooth muscle cell
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    Selected Abstracts

    Activation and induction of cytosolic phospholipase A2 by IL-1, in human tracheal smooth muscle cells: Role of MAPKs/p300 and NF-,B

    JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 5 2010
    Chiang-Wen Lee
    Abstract Cytosolic phospholipase A2 (cPLA2) plays a pivotal role in mediating agonist-induced arachidonic acid (AA) release for prostaglandin (PG) synthesis during inflammation triggered by IL-1,. However, the mechanisms underlying IL-1,-induced cPLA2 expression and PGE2 synthesis in human tracheal smooth muscle cells (HTSMCs) remain unknown. IL-1,-induced cPLA2 protein and mRNA expression, PGE2 production, or phosphorylation of p42/p44 MAPK, p38 MAPK, and JNK1/2, which was attenuated by pretreatment with the inhibitors of MEK1/2 (U0126), p38 MAPK (SB202190), and JNK1/2 (SP600125) or transfection with siRNAs of MEK1, p42, p38, and JNK2. IL-1,-induced cPLA2 expression was also inhibited by pretreatment with a NF-,B inhibitor, helenalin or transfection with siRNA of NIK, IKK,, or IKK,. IL-,-induced NF-,B translocation was blocked by pretreatment with helenalin, but not U0126, SB202190, and SP600125. In addition, transfection with p300 siRNA blocked cPLA2 expression induced by IL-1,. Moreover, p300 was associated with the cPLA2 promoter, which was dynamically linked to histone H4 acetylation stimulated by IL-1,. These results suggest that in HTSMCs, activation of MAPKs, NF-,B, and p300 are essential for IL-1,-induced cPLA2 expression and PGE2 secretion. J. Cell. Biochem. 109: 1045,1056, 2010. © 2010 Wiley-Liss, Inc. [source]

    Interleukin-1, induces MMP-9 expression via p42/p44 MAPK, p38 MAPK, JNK, and nuclear factor-,B signaling pathways in human tracheal smooth muscle cells

    JOURNAL OF CELLULAR PHYSIOLOGY, Issue 3 2007
    Kao-Chih Liang
    Matrix metalloproteinases (MMPs) are responsible for degradation of extracellular matrix and play important roles in cell migration, proliferation, and tissue remodeling related to airway inflammation. Interleukin-1, (IL-1,) has been shown to induce MMP-9 production in many cell types and contribute to airway inflammatory responses. However, the mechanisms underlying MMP-9 expression induced by IL-1, in human tracheal smooth muscle cells (HTSMCs) remain unclear. Here, we investigated the roles of p42/p44 MAPK, p38 MAPK, JNK, and NF-,B pathways for IL-1,-induced MMP-9 production in HTSMCs. IL-1, induced production of MMP-9 protein and mRNA in a time- and concentration-dependent manner determined by zymographic, Western blotting, and RT-PCR analyses, which was attenuated by inhibitors of MEK1/2 (U0126), p38 MAPK (SB202190), JNK (SP600125), and NF-,B (helenalin), and transfection with dominant negative mutants of MEK1/2, p38 and JNK, respectively. IL-1,-stimulated phosphorylation of p42/p44 MAPK, p38 MAPK, and JNK was attenuated by pretreatment with U0126, SB202190, SP600125, or transfection with these dominant negative mutants of MEK, ERK, p38 and JNK, respectively. Furthermore, IL-1,-stimulated translocation of NF-,B into the nucleus and degradation of I,B-, was blocked by helenalin. Finally, the reporter gene assay revealed that MAPKs and NF-,B are required for IL-1,-induced MMP-9 luciferase activity in HTSMCs. MMP-9 promoter activity was enhanced by IL-1, in HTSMCs transfected with MMP-9-Luc, which was inhibited by helenalin, U0126, SB202190, and SP600125. Taken together, the transcription factor NF-,B, p42/p44 MAPK, p38 MAPK, and JNK that are involved in MMP-9 expression in HTSMCs exposed to IL-1, have now been identified. J. Cell. Physiol. 211: 759,770, 2007. © 2007 Wiley-Liss, Inc. [source]

    In vitro tracheal hyperresponsiveness to muscarinic receptor stimulation by carbachol in a rat model of bleomycin-induced pulmonary fibrosis

    AUTONOMIC & AUTACOID PHARMACOLOGY, Issue 3 2006
    J. Barrio
    Summary 1 Bleomycin-induced lung injury is widely used as an experimental model to investigate the pathophysiology of pulmonary fibrosis but the alterations in the pharmacological responsiveness of airways isolated from bleomycin-exposed animals has been scarcely investigated. The aim of this study was to examine the in vitro tracheal responses to muscarinic receptor stimulation with carbachol in a rat bleomycin model. 2 Concentration,response curves to carbachol (10 nm to 0.1 mm) were obtained in tracheal rings isolated from Sprague,Dawley rats 14 days after endotracheal bleomycin or saline. The intracellular calcium signal in response to carbachol (10 ,m) was measured by epifluorescence microscopy using fura-2 in primary cultures of tracheal smooth muscle cells from bleomycin- and saline-exposed rats. Circulating plasma tumour necrosis factor (TNF)- ,/interleukin (IL)-1, levels were measured by enzyme-linked immunosorbent assay. 3 Maximal contraction in response to carbachol was significantly greater in tracheal rings from bleomycin-exposed rats compared with controls (15.8 ± 1.3 mN vs. 11.8 ± 1.4 mN; n = 19, P < 0.05). 4 Carbachol (10 ,m) elicited a transient increase of intracellular calcium with greater increment in tracheal smooth muscle cells from bleomycin-exposed rats compared with controls (372 ± 42 nmvs. 176 ± 20 nm; n = 7, P < 0.01). 5 Circulating plasma levels of TNF- ,/IL-1, were augmented in bleomycin-exposed rats compared with controls. Tissue incubation with TNF- , (100 ng ml,1)/IL-1, (10 ng ml,1) increased in vitro tracheal responsiveness to carbachol. 6 In conclusion, tracheal contraction in response to muscarinic receptor stimulation with carbachol was increased in bleomycin-exposed rats. This in vitro cholinergic hyperresponsiveness may be related to the augmented levels of inflammatory cytokines in bleomycin-exposed rats. [source]