Curcumin inhibits the proliferation of airway smooth muscle cells in vitro and in vivo

Asthma is considered to be a chronic inflammatory disease of the airways and is highlighted by excessive airway narrowing in response to various stimuli. Subepithelial fibrosis and increased airway smooth muscle mass are characteristic pathological features of the disease. Airway remodelling in asthma involves cellular hyperplasia and hypertrophy of bronchial myocytes. Smooth muscle cells from a variety of tissues have been shown to be multifunctional mesenchymal cells capable of expressing considerable phenotypic plasticity in vivo in response to injury and pathological stimuli. The growth response of vascular smooth muscle cells following arterial injury has been fairly well characterized, and it appears many of the chemical mediators responsible are common to the inflamed bronchi seen in asthmatics. Specific studies regarding the effects of phenotypic modulation of airway smooth muscle and the potential contribution of this phenomenon to the pathogenesis of chronic asthma have not been carried out. Limited evidence, some indirect, suggests that contractile properties of smooth muscle from inflamed tissues are altered; if this is the case in asthma, then considerations of the effects of airway smooth muscle hypertrophy should be broadened beyond that of only contributing to bronchial hyperresponsiveness via an increase in bronchial wall thickness. Recruitment and modulation of smooth muscle cells to functionally different phenotypes, which contribute to fibrosis by secreting extracellular matrix materials and promote cellular hyperplasia by producing growth factors, are known to occur in atherogenic blood vessels; and evidence suggests that airway smooth muscle cells might play a similar role in asthma. We report the identification of markers of differentiation for airway smooth muscle cells. These markers should be useful tools in the elucidation of phenotypic heterogeneity of smooth muscle in asthmatic airways and, thereby, allow for the definition of a clearer role for bronchial smooth muscle cells in the pathogenesis of chronic asthma.Key words: airway smooth muscle cells, asthma, phenotype, pathogenesis, proliferation.

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Asthmatic Airway Smooth Muscle Cells Are Insensitive To The In Vitro Effects Of IL-22 On Growth Factor Expression

10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a1399 ◽

2012 ◽

Author(s):

Ibrahim Almaghlouth ◽

Qutayba Hamid ◽

Jill R. Johnson

Keyword(s):

Smooth Muscle ◽

Growth Factor ◽

Smooth Muscle Cells ◽

Airway Smooth Muscle ◽

Muscle Cells ◽

Airway Smooth Muscle Cells ◽

Factor Expression ◽

Growth Factor Expression ◽

In Vitro Effects

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In vivo allergen-activated inflammatory eosinophils reduced airway smooth muscle cells apoptosis in allergic asthma patients

10.1183/13993003.congress-2021.pa694 ◽

2021 ◽

Author(s):

Andrius Januskevicius ◽

Egle Jurkeviciute ◽

Airidas Rimkunas ◽

Jolita Palacionyte ◽

Beatrice Tamasauskaite ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Allergic Asthma ◽

Airway Smooth Muscle ◽

Muscle Cells ◽

Airway Smooth Muscle Cells ◽

Asthma Patients

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Saponins of Dioscorea Nipponicae Inhibits IL-17A-Induced Changes in Biomechanical Behaviors of In Vitro Cultured Human Airway Smooth Muscle Cells

Journal of Engineering and Science in Medical Diagnostics and Therapy ◽

10.1115/1.4042317 ◽

2019 ◽

Vol 2 (1) ◽

Author(s):

Yue Wang ◽

Yifan Zhang ◽

Ming Zhang ◽

Jingjing Li ◽

Yan Pan ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Airway Smooth Muscle ◽

Traction Force ◽

Muscle Cells ◽

Airway Smooth Muscle Cells ◽

Human Airway Smooth Muscle ◽

Human Airway ◽

Induced Changes

Airway hyperresponsiveness (AHR) is one of the main pathologic features of bronchial asthma, which is largely attributable to enhanced contractile response of asthmatic airway smooth muscle. Although β2 adrenergic receptor agonists are commonly used to relax airway smooth muscle for treating AHR, there are side effects such as desensitization of long-term use. Therefore, it is desirable to develop alternative relaxant for airway smooth muscle, preferably based on natural products. One potential candidate is the inexpensive and widely available natural herb saponins of Dioscorea nipponicae (SDN), which has recently been reported to suppress the level of inflammatory factor IL-17A in ovalbumin-induced mice, thereby alleviating the inflammation symptoms of asthma. Here, we evaluated the biomechanical effect of SDN on IL-17A-mediated changes of cultured human airway smooth muscle cells (HASMCs) in vitro. The stiffness and traction force of the cells were measured by optical magnetic twisting cytometry (OMTC), and Fourier transform traction microscopy (FTTM), respectively. The cell proliferation was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) colorimetry, the cell migration was measured by cell scratch test, and the changes of cell cytoskeleton were assessed by laser confocal microscopy. We found that the stiffness and traction force of HASMCs were enhanced along with the increases of IL-17A concentration and exposure time, and SDN treatment dose-dependently reduced these IL-17A-induced changes in cell mechanical properties. Furthermore, SDN alleviated IL-17A-mediated effects on HASMCs proliferation, migration, and cytoskeleton remodeling. These results demonstrate that SDN could potentially be a novel drug candidate as bronchodilator for treating asthma-associated AHR.

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Immunolocalization of a Na-K-2Cl cotransporter in human tracheobronchial smooth muscle

Journal of Applied Physiology ◽

10.1152/japplphysiol.00621.2002 ◽

2003 ◽

Vol 94 (4) ◽

pp. 1596-1601 ◽

Cited By ~ 6

Author(s):

Lynn M. Iwamoto ◽

Kenneth T. Nakamura ◽

Randal K. Wada

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Airway Smooth Muscle ◽

Polyclonal Antibodies ◽

Muscle Cells ◽

Airway Smooth Muscle Cells ◽

Smooth Muscle Function ◽

Normal Human

Inhibition of the Na-K-2Cl (NKCC) cotransporter by loop diuretics is associated with airway relaxation, but there has been no direct evidence for the expression of this protein in airway smooth muscle. Thus we hypothesized that a NKCC cotransporter is present and functional in airway smooth muscle cells. Monoclonal and polyclonal antibodies were used first to demonstrate the presence of a NKCC cotransporter protein in isolated human fetal trachea and normal human bronchial smooth muscle cells (BSMC) by Western blotting. The cotransporter protein was then localized by immunohistochemical staining to airway smooth muscle cells in culture and in situ. The localization was confirmed by indirect immunofluorescence and laser confocal microscopy in the BSMC. Cotransporter function in BSMC was also confirmed in vitro by bumetanide-mediated inhibition of rubidium uptake. Our present findings thus document the presence of a functional NKCC cotransporter in human airway smooth muscle, providing a basis for defining the role of this ion cotransporter in airway smooth muscle function.

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Tea Polyphenols Selectively Inhibit Proliferation and Migration of Airway Smooth Muscle Cells

Journal of Biology and Life Science ◽

10.5296/jbls.v9i2.13018 ◽

2018 ◽

Vol 9 (2) ◽

pp. 39

Author(s):

Mengmeng Yang ◽

Fang Liang ◽

Defeng Xu ◽

Yue Wang ◽

Huan Zhou ◽

...

Keyword(s):

Smooth Muscle ◽

Smooth Muscle Cells ◽

Airway Smooth Muscle ◽

Muscle Cells ◽

Nuclear Factor Κb ◽

Tea Polyphenols ◽

Airway Smooth Muscle Cells ◽

And Migration ◽

Dose Dependent

Airway smooth muscle cells (ASMCs) have been recommended as a target for the treatment of inflammation and narrowing of the airways in asthma. New safe and efficient approaches to relieve symptoms caused by ASMCs is highly desired. Inspired by the inhibitory effects of tea polyphenols on vascular smooth muscle cells (VSMCs), tea polyphenols were applied in the current work to evaluate their regulation of ASMCs in vitro. A dose-dependent decrease of ASMCs density was observed after 24 h incubation with tea polyphenols. Additionally, ASMCs were significantly more sensitive to tea polyphenols than human bronchial epithelial cells (HBECs). Tea polyphenol treatment led to a dose dependent inhibition on ASMC migration and reduced the gene expression of nuclear factor-κB (NF-κB). In studies which compared the four main polyphenolic constituents of tea polyphenols—including epicatechin (EC), epicatechingallate (ECG), epigallocatechin (EGC) and epigallocatechingallate (EGCG)—on the proliferation of ASMCs, EGC was identified as being the most potent. These results suggest tea polyphenols are a promising agent for ASMCs targeted asthma control.

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