Alveolar Epithelial Type I Cells Express β2-Adrenergic Receptors and G-protein Receptor Kinase 2

Liebler, Janice M.; Borok, Zea; Li, Xian; Zhou, Baosen; Sandoval, Argelia; Kim, Kwang‐Jin; Crandall, Edward D.

doi:10.1369/jhc.3a6184.2004

Cited by 26 publications

(23 citation statements)

References 37 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Using an RT-I40 antibody specific for type 1 cells (provided by Dr. Leland Dobbs), we show that after 72 h in culture the cell lysates collected become increasingly immunoreactive with RT-I40 antibody. Several groups have verified that type 2 cells can transdifferentiate into alveolar type 1 cells when maintained in culture (2,11,25). Although the data are not shown, we also confirmed that when type 2 cells remain in culture past day 3, expression of surfactant proteins also significantly decrease.…”

Section: Immunolocalization Of Alveolar Cells For Patch Clamp Analysisupporting

confidence: 81%

Redox Regulation of Epithelial Sodium Channels Examined in Alveolar Type 1 and 2 Cells Patch-clamped in Lung Slice Tissue

Helms

Jain

Self

et al. 2008

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

Section: Immunolocalization Of Alveolar Cells For Patch Clamp Analysisupporting

confidence: 81%

Redox Regulation of Epithelial Sodium Channels Examined in Alveolar Type 1 and 2 Cells Patch-clamped in Lung Slice Tissue

Helms

Jain

Self

et al. 2008

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Although both b 1 and b 2 subtypes coexist and are distributed uniformly in the alveolar walls, the b 2 -subtype predominates (70%) (4). Isolated rat alveolar type II cells possess b 2 AR and data from autoradiographic and immunohistochemical studies support their presence in the alveolar type 1 cells (4,5).…”

Section: B-adrenergic Receptors Subtypes and Distribution In The Lungmentioning

confidence: 84%

“…Thus, b 2 AR agonists increase Na 1 flux across the apical cell membrane by increasing both membrane-bound channel abundance and Na 1 flux through the channels. Data supporting this conclusion come primarily from rat alveolar type II cells; however, the observation that alveolar type I cells have functional ion transporters and b 2 AR suggests similar regulation of ion transport in alveolar type I cells (5,56,57). Activation of b 2 -adrenergic receptor increases cellular Na,KATPase activity in alveolar epithelial cells in vitro and lung tissue (8,39,49,58).…”

Section: Role Of Alveolar Epithelial B 2 -Adrenergic Receptorsmentioning

confidence: 96%

Alveolar Epithelial β₂-Adrenergic Receptors

Mutlu

Factor²

2008

Am J Respir Cell Mol Biol

View full text Add to dashboard Cite

b 2 -adrenergic receptors are present throughout the lung, including the alveolar airspace, where they play an important role for regulation of the active Na 1 transport needed for clearance of excess fluid out of alveolar airspace. b 2 -adrenergic receptor signaling is required for up-regulation of alveolar epithelial active ion transport in the setting of excess alveolar edema. The positive, protective effects of b 2 -adrenergic receptor signaling on alveolar active Na 1 transport in normal and injured lungs provide substantial support for the use of b-adrenergic agonists to accelerate alveolar fluid clearance in patients with cardiogenic and noncardiogenic pulmonary edema. In this review, we summarize the role of b 2 -adrenergic receptors in the alveolar epithelium with emphasis on their role in the regulation of alveolar active Na 1 transport in normal and injured lungs.Keywords: pulmonary edema; acute respiratory distress syndrome; acute lung injury; alveoli; albuterol b 2 -adrenergic receptors (b 2 AR) are present throughout the lung. In the alveolar airspace they are important for regulation of the active Na 1 transport needed for clearance of excess fluid out of alveolar airspace (1). Both experimental and limited clinical data suggest that b-adrenergic agonists working via the b 2 AR accelerate clearance of excess fluid from the alveolar airspace, creating the possibility of their use for treatment of pulmonary edema and acute lung injury (ALI).In this review, we summarize the role of b 2 -adrenergic receptors in the alveolar epithelium with emphasis on their role in regulation of alveolar active Na 1 transport in normal and injured lungs. We also overview data regarding b 2 -agonist therapy for pulmonary edema and lung injury. In the lung, b2-adrenergic receptor (b 2 AR) expression increases with each airway generation, with the greatest total amounts in the distal airways and alveoli (3). Greater than 90% of all b-adrenergic receptors in human lung are located in the alveoli (4). Although both b 1 and b 2 subtypes coexist and are distributed uniformly in the alveolar walls, the b 2 -subtype predominates (70%) (4). Isolated rat alveolar type II cells possess b 2 AR and data from autoradiographic and immunohistochemical studies support their presence in the alveolar type 1 cells (4, 5). -Adrenergic Receptor Structure and FunctionThe b 2 -adrenergic receptor is a 1,200-base pair, single-copy, intronless gene located on the long arm of human chromosome 5 that encodes a 413-amino acid protein with a molecular mass of approximately 46.5 kD (1). The b 2 -receptor is a prototypical G protein-coupled receptor (GPCR) with seven-transmembrane domains, an extracellular amino terminus, an intracellular carboxyl terminus, three interconnecting extracellular loops, and three intracellular loops.b 2 -adrenergic receptors exist in the plasma membrane in an equilibrium between at least two structural conformations; inactive and active forms that are defined based on their ability to associate with the stimulatory guano...

show abstract

“…many pro-inflammatory and immune cells, including mast cells [35], macrophages [36], neutrophils [37], lymphocytes [38], eosinophils [39], epithelial and endothelial cells [40,41], and both type I and type II alveolar cells [10,42,43]. Thus, many cell types within the lung that are implicated in the pathogenesis of asthma are potential targets of inhaled b 2 -adrenoceptor agonists.…”

Section: Adrenoceptors In the Lungmentioning

confidence: 99%

Beyond the dogma: novel 2-adrenoceptor signalling in the airways

Giembycz

Newton²

2006

European Respiratory Journal

132

118

View full text Add to dashboard Cite

b 2 -Adrenoceptor agonists evoke rapid bronchodilatation and are the mainstay of the treatment of asthma symptoms worldwide. The mechanism of action of this class of compounds is believed to involve the stimulation of adenylyl cyclase and subsequent activation of the cyclic adenosine monosphosphate (cAMP)/cAMP-dependent protein kinase cascade.This classical model of b 2 -adrenoceptor-mediated signal transduction is deeply entrenched, but there is compelling evidence that agonism of b 2 -adrenoceptors can lead to the activation of multiple effector pathways, which now compels researchers in academia and the pharmaceutical industry alike to think beyond the traditional dogma. Therefore, the regulation by b 2 -adrenoceptor agonists of responses, including airways smooth muscle tone and the secretory capacity of the epithelium and pro-inflammatory/immune cells, may be highly complex, involving both cAMPdependent and -independent mechanisms that, in many cases, may act in concert.In this article, the current status of b 2 -adrenoceptor-mediated signalling in the airways is reviewed in the context of understanding mechanisms that may underlie both the beneficial and detrimental effects of these drugs in asthma symptom management.

show abstract

Alveolar Epithelial Type I Cells Express β2-Adrenergic Receptors and G-protein Receptor Kinase 2

Cited by 26 publications

References 37 publications

Redox Regulation of Epithelial Sodium Channels Examined in Alveolar Type 1 and 2 Cells Patch-clamped in Lung Slice Tissue

Redox Regulation of Epithelial Sodium Channels Examined in Alveolar Type 1 and 2 Cells Patch-clamped in Lung Slice Tissue

Alveolar Epithelial β₂-Adrenergic Receptors

Beyond the dogma: novel 2-adrenoceptor signalling in the airways

Contact Info

Product

Resources

About

Alveolar Epithelial Type I Cells Express β2-Adrenergic Receptors and G-protein Receptor Kinase 2

Cited by 26 publications

References 37 publications

Redox Regulation of Epithelial Sodium Channels Examined in Alveolar Type 1 and 2 Cells Patch-clamped in Lung Slice Tissue

Redox Regulation of Epithelial Sodium Channels Examined in Alveolar Type 1 and 2 Cells Patch-clamped in Lung Slice Tissue

Alveolar Epithelial β2-Adrenergic Receptors

Beyond the dogma: novel 2-adrenoceptor signalling in the airways

Contact Info

Product

Resources

About

Alveolar Epithelial β₂-Adrenergic Receptors