A human airway smooth muscle cell line that retains physiological responsiveness

Panettieri, RA; Murray, Richard; DePalo, Louis; Yadvish, P. A.; Kotlikoff, Michael I.

doi:10.1152/ajpcell.1989.256.2.c329

Cited by 295 publications

(256 citation statements)

References 13 publications

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“…HASM cells were isolated from the trachealis muscles of unused human lung alographs, in accordance with guidelines of the Committee on Studies Involving Human Beings at the University of Pennsylvania, as described elsewhere (12)(13)(14) and in METHODS in the online supplement. HASM cells were plated on tissue culture-treated plastic at a density of 1.0 3 10 4 cells/cm 2 in Ham's F-12 medium, supplemented with 10% FBS and antibiotics.…”

Section: Isolation Of Primary Hasm Cellsmentioning

confidence: 99%

Polycyclic Aromatic Hydrocarbons Impair Function of β₂-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells

Factor

Akhmedov

McDonald

et al. 2011

Am J Respir Cell Mol Biol

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Incomplete combustion produces a pollutant mixture that includes polycyclic aromatic hydrocarbons (PAHs). Previous work by the Columbia Center for Children's Environmental Health (CCCEH) and others linked exposure to PAH with symptoms of asthma and other adverse health effects in young children. Inhaled b 2 -adrenergic agonists are mainstays in the treatment of reactive airway diseases. These exogenous catecholamines engage membrane-bound b 2 -adrenergic receptors (b 2 AR) on airway epithelial and smooth muscle cells to cause airway dilation. We hypothesized that exposure to PAH might similarly interfere with the function of b 2 AR in airway epithelial or smooth muscle cells, reducing the efficacy of a medication important for the treatment of asthma symptoms. A PAH mixture was devised, based on ambient levels measured prenatally among a cohort of pregnant women participating at the CCCEH. Primary airway epithelial and smooth muscle cells were exposed to varying concentrations of the PAH mixture, and expression, function, and signaling of b 2 AR were assessed. Murine tracheal epithelial cells and human airway smooth muscle cells, after exposure to a PAH mixture, exhibited reduced expression and function of b 2 AR. These findings support our hypothesis that environmentally relevant PAHs can impede b 2 AR-mediated airway relaxation, and suggest a new paradigm where air pollutants not only contribute to the pathogenesis of childhood asthma, but also diminish responsiveness to standard therapy.

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Section: Isolation Of Primary Hasm Cellsmentioning

confidence: 99%

Polycyclic Aromatic Hydrocarbons Impair Function of β₂-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells

Factor

Akhmedov

McDonald

et al. 2011

Am J Respir Cell Mol Biol

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“…Cells were seeded on 96-well plates and growth arrested by incubating the cultures in serum-free medium. Confluent, growth-arrested cells were used because cells can be synchronized in the G 0 -G 1 phase of the cell cycle (43). After 24 h in serum-free medium, the cells were stimulated with either recombinant human activin A (1, 10, or 100 ng/ml) (R&D Systems) or hEGF (100 ng/ml) (R&D Systems).…”

Section: Hasmc Culture and Proliferation Assaymentioning

confidence: 99%

Regulation of Activin A Expression in Mast Cells and Asthma: Its Effect on the Proliferation of Human Airway Smooth Muscle Cells

Cho¹,

Yao²,

Wang³

et al. 2003

The Journal of Immunology

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Activin A, a homodimeric protein (βAβA) and a member of the TGF-β superfamily, is involved in the inflammatory repair process. Using cDNA microarray analysis, we discovered strong induction of the activin βA gene in human mast cells (MC) on stimulation with PMA and calcium ionophore (A23187). Activin βA mRNA was also highly induced in primary cultured murine bone marrow MC (BMMC) after stimulation by IgE receptor cross-linking. Secretion of activin A was evident in human mast cell-1 line cells 3 h after stimulation and progressively increased over time. Activin A was present in the cytoplasm of activated but not unstimulated murine bone marrow MC as demonstrated by immunofluorescence studies, suggesting that secretion of activin A by MC was due to de novo synthesis rather than secretion of preformed protein. Activin A also colocalized with human lung MC from patients with asthma by double-immunofluorescence staining. Furthermore, secretion of activin A was significantly increased in the airway of wild-type mice after OVA sensitization followed by intranasal challenge. Secretion of activin A, however, was greatly reduced in MC-deficient WBB6F1-W/Wv mice as compared with wild-type mice, indicating that MC are an important contributor of activin A in the airways of a murine asthma model. Additionally, activin A promoted the proliferation of human airway smooth muscle cells. Taken together, these data suggest that MC-derived activin A may play an important role in the process of airway remodeling by promoting the proliferation of airway smooth muscle.

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“…HASM cells were isolated from tracheal muscle of lung transplant donors, approved by the University of Pennsylvania Committee on Studies Involving Human Beings (26). The cells were serum deprived in IT medium (i.e., the medium containing 5.7 g/ml insulin and 5 g/ml transferrin) for 2 days before the experiments.…”

Section: Cell Culture and Experimental Protocolmentioning

confidence: 99%

Spatial and temporal traction response in human airway smooth muscle cells

Tolic-Norrelykke

Butler

Chen

et al. 2002

American Journal of Physiology-Cell Physiology

124

104

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. Spatial and temporal traction response in human airway smooth muscle cells. Am J Physiol Cell Physiol 283: C1254-C1266, 2002. First published June 26, 2002 10.1152/ajpcell.00169.2002Tractions that cells exert on their substrates are essential in cell spreading, migration, and contraction. These tractions can be determined by plating the cells on a flexible gel and measuring the deformation of the gel by using fluorescent beads embedded just below the surface of the gel. In this article we describe the image correlation method (ICM) optimized for determining the displacement field of the gel under a contracting cell. For the calculation of the traction field from the displacement field we use the recently developed method of Fourier transform traction cytometry (FTTC). The ICM and FTTC methods are applied to human airway smooth muscle cells during stimulation with the contractile agonist histamine or the relaxing agonist isoproterenol. The overall intensity of the cell contraction (the median traction magnitude, the energy transferred from the cell to the gel, and the net contractile moment) increased after activation with histamine, and decreased after treatment with isoproterenol. Cells exhibited regional differences in the time course of traction during the treatment. Both temporal evolution and magnitude of traction increase induced by histamine varied markedly among different cell protrusions, whereas the nuclear region showed the smallest response. These results suggest that intracellular mediators of cell adhesion and contraction respond to contractile stimuli with different rates and intensities in different regions of the cell.

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A human airway smooth muscle cell line that retains physiological responsiveness

Cited by 295 publications

References 13 publications

Polycyclic Aromatic Hydrocarbons Impair Function of β₂-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells

Polycyclic Aromatic Hydrocarbons Impair Function of β₂-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells

Regulation of Activin A Expression in Mast Cells and Asthma: Its Effect on the Proliferation of Human Airway Smooth Muscle Cells

Spatial and temporal traction response in human airway smooth muscle cells

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A human airway smooth muscle cell line that retains physiological responsiveness

Cited by 295 publications

References 13 publications

Polycyclic Aromatic Hydrocarbons Impair Function of β2-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells

Polycyclic Aromatic Hydrocarbons Impair Function of β2-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells

Regulation of Activin A Expression in Mast Cells and Asthma: Its Effect on the Proliferation of Human Airway Smooth Muscle Cells

Spatial and temporal traction response in human airway smooth muscle cells

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Product

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Polycyclic Aromatic Hydrocarbons Impair Function of β₂-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells

Polycyclic Aromatic Hydrocarbons Impair Function of β₂-Adrenergic Receptors in Airway Epithelial and Smooth Muscle Cells