Regulation of ciliary beat frequency by both PKA and PKG in bovine airway epithelial cells

Wyatt, Todd A.; Spurzem, John R.; May, Kathy; Sisson, Joseph H.

doi:10.1152/ajplung.1998.275.4.l827

Cited by 92 publications

(149 citation statements)

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“…Such a calcium-mediated pathway via PKC might be responsible for the change in baseline beating observed in response to the combination of isoproterenol and ethanol. Cyclic GMP and PKG also have been implicated as regulators of CBF (Wyatt et al, 1998;Li et al, 2000;Zagoory et al, 2002). In the rat model, we observed no significant changes in baseline or isoproterenol-stimulated PKG activity in the tracheal epithelial cells of smoke-or sham-exposed rats ingesting any ethanol concentration.…”

Section: Discussionmentioning

confidence: 48%

“…In this model, ethanol requires an adenosine 3':5'-cyclic monophosphate (cAMP) and nitric oxide-dependent signaling pathway (Sisson et al, 1999;Wyatt et al, 2003). This follows the observation that either cAMP or cyclic guanosine monophosphate (cGMP) elevations result in increased cilia beating (Wyatt et al, 1998). However, continued exposure to ethanol eventually results in a return to baseline, unstimulated levels of cilia beating as potentially mediated via the action of a cAMP-phosphodiesterase (Forgèt et al, 2003).…”

mentioning

confidence: 84%

“…The remaining trachea were opened by a longitudinal incision and washed in M-199, and epithelial cells were extracted with a sterile cell lifter (Fisher, Springfield, NJ). Extracted tracheal epithelial cells were flash frozen with liquid nitrogen in a cell lysis buffer as previously described (Wyatt et al, 1998).…”

Section: Tissue Preparationmentioning

confidence: 99%

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Desensitization of PKA‐Stimulated Ciliary Beat Frequency in an Ethanol‐Fed Rat Model of Cigarette Smoke Exposure

Wyatt

Gentry-Nielsen

Pavlik

et al. 2004

Alcoholism Clin & Exp Res

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Background-Our previous studies have shown that the ciliary beat frequency (CBF) of cultured ciliated airway epithelial cells exposed to chronic ethanol fails to increase in response to β-agonist stimulation. This loss of the ciliary "flight response" correlates with an ethanol-mediated desensitization of adenosine 3':5'-cyclic monophosphate-dependent protein kinase (PKA), a known regulatory component of CBF stimulation. We hypothesized that a similar ethanol-mediated desensitization of CBF would occur in vivo.

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Section: Discussionmentioning

confidence: 48%

mentioning

confidence: 84%

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Desensitization of PKA‐Stimulated Ciliary Beat Frequency in an Ethanol‐Fed Rat Model of Cigarette Smoke Exposure

Wyatt

Gentry-Nielsen

Pavlik

et al. 2004

Alcoholism Clin & Exp Res

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“…However, isoproterenol-stimulated CBF increases in control lamb tracheal rings were not observed in tracheal rings obtained from ethanol-exposed lambs. Because isoproterenol-stimulated CBF increases require the activation of PKA (Wyatt et al, 1998) epithelial cell PKA activity was also assayed in this study. Isoproterenol significantly increased PKA activity in control trachea, but failed to activate PKA in ethanol-exposed trachea ( Figure 2B).…”

Section: Cbf Resultsmentioning

confidence: 99%

Maternal alcohol ingestion reduces surfactant protein A expression by preterm fetal lung epithelia

Lazic¹,

Wyatt²,

Matić³

et al. 2007

Alcohol

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In addition to neurodevelopmental effects, alcohol consumption at high levels during pregnancy is associated with immunomodulation and premature birth. Premature birth, in turn, is associated with increased susceptibility to various infectious agents such as Respiratory Syncytial Virus (RSV). The initial line of pulmonary innate defense includes the mucociliary apparatus, which expels microorganisms trapped within the airway secretions. Surfactant proteins A and D (SP-A and SP-D, respectively) are additional components of pulmonary innate immunity and have an important role in pulmonary defense against inhaled pathogens. The purpose of this study was to determine if chronic alcohol consumption during the third trimester of pregnancy alters the function of the mucociliary apparatus and expression of SP-A and SP-D of fetal lung epithelia. Sixteen, date-mated ewes were assigned to two different groups; an ethanol exposed group in which ewes received ethanol through surgically implanted intra-abomasal cannula during the third trimester of pregnancy, and a control group in which ewes received the equivalent amount of water instead of ethanol. Within these two groups, ewes were further randomly assigned to a full-term group in which the lambs were naturally delivered, and a pre-term group in which the lambs were delivered prematurely via an abdominal incision and uterotomy. Ethanol was administered 5 times a week as a 40% solution at 1gr/kg of body weight. The mean maternal serum alcohol concentration (SAC) measured 6 hr post administration was 16.3 +/− 4.36 mg/dL. Tracheas from 6 full-term lambs were collected to assess ciliary beat frequency (CBF). The lung tissue from all (24) lambs was collected for immunohistochemistry (IHC) analysis of SP-A and SP-D protein production and fluorogenic realtime quantitative polymerase chain reaction analysis (qPCR) of SP-A and SP-D mRNA levels. Exposure to ethanol during pregnancy significantly blocked stimulated increase in CBF though ethanol-mediated desensitization of cAMP-dependant protein kinase (PKA). In addition, pre-term born/ethanol-exposed lambs showed significantly decreased SP-A m-RNA expression when compared to the pre-term born/control group (p=0.004); no significant changes were seen with SP-D. The full-term/ethanol exposed lambs had no significant alterations in mRNA levels, but had significantly less detectable SP-A protein when compared to the full-term/control lambs (p=0.02).Corresponding author: Tatjana Lazic, DVM, MS, 2740 Veterinary Medicine, Department of Veterinary Pathology, Iowa State University, Ames, Iowa 50011-1250, 515-294-6688, FAX 515-294-5423, tlazic@iastate.edu. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process error...

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“…The cAMP-dependent PKA is established as an important regulator of the cilia stimulation pathway (2,42,51,62). To determine the mechanism of NECA-stimulation of CBF, we measured PKA activity in our primary ciliated BBEC model.…”

Section: L174 Adenosine Receptor Activation In Epithelial Ciliary Motmentioning

confidence: 99%

Adenosine activation of A_2Breceptor(s) is essential for stimulated epithelial ciliary motility and clearance

Allen‐Gipson¹,

Blackburn

Schneider

et al. 2011

American Journal of Physiology-Lung Cellular and Molecular Phys

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sine activation of A2B receptor(s) is essential for stimulated epithelial ciliary motility and clearance. Am J Physiol Lung Cell Mol Physiol 301: L171-L180, 2011. First published May 27, 2011 doi:10.1152/ajplung.00203.2010.-Mucociliary clearance, vital to lung clearance, is dependent on cilia beat frequency (CBF), coordination of cilia, and the maintenance of periciliary fluid. Adenosine, the metabolic breakdown product of ATP, is an important modulator of ciliary motility. However, the contributions of specific adenosine receptors to key airway ciliary motility processes are unclear. We hypothesized that adenosine modulates ciliary motility via activation of its cell surface receptors (A1, A2A, A2B, or A3). To test this hypothesis, mouse tracheal rings (MTRs) excised from wild-type and adenosine receptor knockout mice (A1, A2A, A2B, or A3, respectively), and bovine ciliated bronchial epithelial cells (BBECs) were stimulated with known cilia activators, isoproterenol (ISO; 10 M) and/or procaterol (10 M), in the presence or absence of 5=-(Nethylcarboxamido) adenosine (NECA), a nonselective adenosine receptor agonist [100 nM (A1, A2A, A3); 10 M (A2B)], and CBF was measured. Cells and MTRs were also stimulated with NECA (100 nM or 10 M) in the presence and absence of adenosine deaminase inhibitor, erythro-9-(2-hydroxy-3-nonyl) adenine hydrochloride (10 M). Both ISO and procaterol stimulated CBF in untreated cells and/or MTRs from both wild-type and adenosine knockout mice by ϳ3 Hz. Likewise, CBF significantly increased ϳ2-3 Hz in BBECs and wild-type MTRs stimulated with NECA. MTRs from A1, A2A, and A3 knockout mice stimulated with NECA also demonstrated an increase in CBF. However, NECA failed to stimulate CBF in MTRs from A2B knockout mice. To confirm the mechanism by which adenosine modulates CBF, protein kinase activity assays were conducted. The data revealed that NECA-stimulated CBF is mediated by the activation of cAMP-dependent PKA. Collectively, these data indicate that purinergic stimulation of CBF requires A2B adenosine receptor activation, likely via a PKA-dependent pathway. mucociliary clearance; knockout mouse model; bovine bronchial epithelial cells MUCOCILIARY TRANSPORT is an important host defense mechanism in the lung by which the coordinated beating of cilia continuously clears the lung of aspirated microorganisms and inhaled debris. This transport is dependent on the ciliary motion of airway epithelium, physicochemical properties of periciliary fluid, and mucus secretion (45, 50). Regulation of airway ciliary motility is critical because mucociliary transport is considered the first line of defense between the lung and the environment. Stressful conditions such as exercise or inflammation cause cilia in the airway to beat faster, increase clearance, and move an increased number of inhaled particles (2). As a consequence, mucociliary transport is a regulable host defense that can be activated under numerous conditions. It has been well described that ATP, a signaling molecule released by the airw...

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Regulation of ciliary beat frequency by both PKA and PKG in bovine airway epithelial cells

Cited by 92 publications

References 53 publications

Desensitization of PKA‐Stimulated Ciliary Beat Frequency in an Ethanol‐Fed Rat Model of Cigarette Smoke Exposure

Desensitization of PKA‐Stimulated Ciliary Beat Frequency in an Ethanol‐Fed Rat Model of Cigarette Smoke Exposure

Maternal alcohol ingestion reduces surfactant protein A expression by preterm fetal lung epithelia

Adenosine activation of A_2Breceptor(s) is essential for stimulated epithelial ciliary motility and clearance

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Regulation of ciliary beat frequency by both PKA and PKG in bovine airway epithelial cells

Cited by 92 publications

References 53 publications

Desensitization of PKA‐Stimulated Ciliary Beat Frequency in an Ethanol‐Fed Rat Model of Cigarette Smoke Exposure

Desensitization of PKA‐Stimulated Ciliary Beat Frequency in an Ethanol‐Fed Rat Model of Cigarette Smoke Exposure

Maternal alcohol ingestion reduces surfactant protein A expression by preterm fetal lung epithelia

Adenosine activation of A2Breceptor(s) is essential for stimulated epithelial ciliary motility and clearance

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Adenosine activation of A_2Breceptor(s) is essential for stimulated epithelial ciliary motility and clearance