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Adenosine activation of A(2B) receptor(s) is essential for stimulated epithelial ciliary motility and clearance.
Am J Physiol Lung Cell Mol Physiol. 2011 Aug; 301(2):L171-80.AJ

Abstract

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 (A(1), A(2A), A(2B), or A(3)). To test this hypothesis, mouse tracheal rings (MTRs) excised from wild-type and adenosine receptor knockout mice (A(1), A(2A), A(2B), or A(3), respectively), and bovine ciliated bronchial epithelial cells (BBECs) were stimulated with known cilia activators, isoproterenol (ISO; 10 μM) and/or procaterol (10 μM), in the presence or absence of 5'-(N-ethylcarboxamido) adenosine (NECA), a nonselective adenosine receptor agonist [100 nM (A(1), A(2A), A(3)); 10 μM (A(2B))], and CBF was measured. Cells and MTRs were also stimulated with NECA (100 nM or 10 μM) in the presence and absence of adenosine deaminase inhibitor, erythro-9- (2-hydroxy-3-nonyl) adenine hydrochloride (10 μM). Both ISO and procaterol stimulated CBF in untreated cells and/or MTRs from both wild-type and adenosine knockout mice by ~3 Hz. Likewise, CBF significantly increased ~2-3 Hz in BBECs and wild-type MTRs stimulated with NECA. MTRs from A(1), A(2A), and A(3) knockout mice stimulated with NECA also demonstrated an increase in CBF. However, NECA failed to stimulate CBF in MTRs from A(2B) 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 A(2B) adenosine receptor activation, likely via a PKA-dependent pathway.

Authors+Show Affiliations

Division of Pulmonary, Critical Care, Sleep & Allergy, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68198-5910, USA. dallengipson@unmc.eduNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

21622845

Citation

Allen-Gipson, Diane S., et al. "Adenosine Activation of A(2B) Receptor(s) Is Essential for Stimulated Epithelial Ciliary Motility and Clearance." American Journal of Physiology. Lung Cellular and Molecular Physiology, vol. 301, no. 2, 2011, pp. L171-80.
Allen-Gipson DS, Blackburn MR, Schneider DJ, et al. Adenosine activation of A(2B) receptor(s) is essential for stimulated epithelial ciliary motility and clearance. Am J Physiol Lung Cell Mol Physiol. 2011;301(2):L171-80.
Allen-Gipson, D. S., Blackburn, M. R., Schneider, D. J., Zhang, H., Bluitt, D. L., Jarrell, J. C., Yanov, D., Sisson, J. H., & Wyatt, T. A. (2011). Adenosine activation of A(2B) receptor(s) is essential for stimulated epithelial ciliary motility and clearance. American Journal of Physiology. Lung Cellular and Molecular Physiology, 301(2), L171-80. https://doi.org/10.1152/ajplung.00203.2010
Allen-Gipson DS, et al. Adenosine Activation of A(2B) Receptor(s) Is Essential for Stimulated Epithelial Ciliary Motility and Clearance. Am J Physiol Lung Cell Mol Physiol. 2011;301(2):L171-80. PubMed PMID: 21622845.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Adenosine activation of A(2B) receptor(s) is essential for stimulated epithelial ciliary motility and clearance. AU - Allen-Gipson,Diane S, AU - Blackburn,Michael R, AU - Schneider,Daniel J, AU - Zhang,Hui, AU - Bluitt,DeAndre L, AU - Jarrell,Justin C, AU - Yanov,Daniel, AU - Sisson,Joseph H, AU - Wyatt,Todd A, Y1 - 2011/05/27/ PY - 2011/5/31/entrez PY - 2011/5/31/pubmed PY - 2011/9/29/medline SP - L171 EP - 80 JF - American journal of physiology. Lung cellular and molecular physiology JO - Am J Physiol Lung Cell Mol Physiol VL - 301 IS - 2 N2 - 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 (A(1), A(2A), A(2B), or A(3)). To test this hypothesis, mouse tracheal rings (MTRs) excised from wild-type and adenosine receptor knockout mice (A(1), A(2A), A(2B), or A(3), respectively), and bovine ciliated bronchial epithelial cells (BBECs) were stimulated with known cilia activators, isoproterenol (ISO; 10 μM) and/or procaterol (10 μM), in the presence or absence of 5'-(N-ethylcarboxamido) adenosine (NECA), a nonselective adenosine receptor agonist [100 nM (A(1), A(2A), A(3)); 10 μM (A(2B))], and CBF was measured. Cells and MTRs were also stimulated with NECA (100 nM or 10 μM) in the presence and absence of adenosine deaminase inhibitor, erythro-9- (2-hydroxy-3-nonyl) adenine hydrochloride (10 μM). Both ISO and procaterol stimulated CBF in untreated cells and/or MTRs from both wild-type and adenosine knockout mice by ~3 Hz. Likewise, CBF significantly increased ~2-3 Hz in BBECs and wild-type MTRs stimulated with NECA. MTRs from A(1), A(2A), and A(3) knockout mice stimulated with NECA also demonstrated an increase in CBF. However, NECA failed to stimulate CBF in MTRs from A(2B) 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 A(2B) adenosine receptor activation, likely via a PKA-dependent pathway. SN - 1522-1504 UR - https://www.unboundmedicine.com/medline/citation/21622845/Adenosine_activation_of_A_2B__receptor_s__is_essential_for_stimulated_epithelial_ciliary_motility_and_clearance_ L2 - https://journals.physiology.org/doi/10.1152/ajplung.00203.2010?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -