Document Detail


Cystic fibrosis and the relationship between mucin and chloride secretion by cultures of human airway gland mucous cells.
MedLine Citation:
PMID:  21724859     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We investigated how cystic fibrosis (CF) alters the relationship between Cl(-) and mucin secretion in cultures of non-CF and CF human tracheobronchial gland mucous (HTGM and CFTGM, respectively) cells. Biochemical studies showed that HTMG cells secreted typical airway mucins, and immunohistochemical studies showed that these cells expressed MUC1, MUC4, MUC5B, MUC8, MUC13, MUC16, and MUC20. Effects of cumulative doses of methacholine (MCh), phenylephrine (Phe), isoproterenol (Iso), and ATP on mucin and Cl(-) secretion were studied on HTGM and CFTGM cultures. Baseline mucin secretion was not significantly altered in CFTGM cells, and the increases in mucin secretion induced by mediators were unaltered (Iso, Phe) or slightly decreased (MCh, ATP). Across mediators, there was no correlation between the maximal increases in Cl(-) secretion and mucin secretion. In HTGM cells, the Cl(-) channel blocker, diphenylamine-2-carboxylic acid, greatly inhibited Cl(-) secretion but did not alter mucin release. In HTGM cells, mediators (10(-5) M) increased mucin secretion in the rank order ATP > Phe = Iso > MCh. They increased Cl(-) secretion in the sequence ATP > MCh ≈ Iso > Phe. The responses in Cl(-) secretion to MCh, ATP, and Phe were unaltered by CF, but the response to Iso was greatly reduced. We conclude that mucin secretion by cultures of human tracheobronchial gland cells is independent of Cl(-) secretion, at baseline, and is unaltered in CF; that the ratio of Cl(-) secretion to mucus secretion varies markedly depending on mediator; and that secretions induced by stimulation of β-adrenergic receptors will be abnormally concentrated in CF.
Authors:
Walter E Finkbeiner; Lorna T Zlock; Masatoshi Morikawa; Anna Y Lao; Vijay Dasari; Jonathan H Widdicombe
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-07-01
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  301     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-09-30     Completed Date:  2011-12-19     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L402-14     Citation Subset:  IM    
Affiliation:
Department of Pathology, University of California, San Francisco, 94110, USA. walter.finkbeiner@ucsf.edu
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / pharmacology
Adrenergic alpha-1 Receptor Agonists / pharmacology
Adrenergic beta-Agonists / pharmacology
Adult
Bronchi / drug effects*,  pathology
Bronchoconstrictor Agents / pharmacology
Calcium Channel Blockers / pharmacology
Chlorides / metabolism*
Cystic Fibrosis / metabolism*,  pathology,  physiopathology
Cystic Fibrosis Transmembrane Conductance Regulator / metabolism*
Exocrine Glands / drug effects*,  pathology
Humans
Ion Transport / drug effects*
Isoproterenol / pharmacology
Methacholine Chloride / pharmacology
Mucins / secretion*
Phenylephrine / pharmacology
Primary Cell Culture
Respiratory Mucosa / drug effects*,  pathology
Trachea / drug effects*,  pathology
ortho-Aminobenzoates / pharmacology
Grant Support
ID/Acronym/Agency:
DK72517/DK/NIDDK NIH HHS; HL73856/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adrenergic alpha-1 Receptor Agonists; 0/Adrenergic beta-Agonists; 0/Bronchoconstrictor Agents; 0/Calcium Channel Blockers; 0/Chlorides; 0/Mucins; 0/ortho-Aminobenzoates; 126880-72-6/Cystic Fibrosis Transmembrane Conductance Regulator; 56-65-5/Adenosine Triphosphate; 59-42-7/Phenylephrine; 62-51-1/Methacholine Chloride; 7683-59-2/Isoproterenol; 91-40-7/fenamic acid
Comments/Corrections

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