Linked Life Data

19213873

Source:http://linkedlifedata.com/resource/pubmed/id/19213873

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2009-10-21
pubmed:abstractText
ATP is a paracrine regulator of critical airway epithelial cell functions, but the mechanism of its release is poorly understood. Pannexin (Panx) proteins, related to invertebrate innexins, form channels (called pannexons) that are able to release ATP from several cell types. Thus, ATP release via pannexons was examined in airway epithelial cells. Quantitative RT-PCR showed Panx1 expression in normal human airway epithelial cells during redifferentiation at the air-liquid interface (ALI), at a level comparable to that of alveolar macrophages; Panx3 was not expressed. Immunohistochemistry showed Panx1 expression at the apical pole of airway epithelia. ALI cultures exposed to hypotonic stress released ATP to an estimated maximum of 255 (+/-64) nM within 1 minute after challenge (n = 6 cultures from three different lungs) or to approximately 1.5 (+/-0.4) microM, recalculated to a normal airway surface liquid volume. Using date- and culture-matched cells (each n > or = 16 from 4 different lungs), the pannexon inhibitors carbenoxolone (10 microM) and probenecid (1 mM), but not the connexon inhibitor flufenamic acid (100 microM), inhibited ATP release by approximately 60%. The drugs affected Panx1 currents in Xenopus oocytes expressing exogenous Panx1 correspondingly. In addition, suppression of Panx1 expression using lentivirus-mediated production of shRNA in differentiated airway epithelial cells inhibited ATP release upon hypotonic stress by approximately 60% as well. These data not only show that Panx1 is expressed apically in differentiated airway epithelial cells but also that it contributes to ATP release in these cells.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1535-4989
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
41
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
525-34
pubmed:dateRevised
2011-1-3
pubmed:meshHeading
pubmed-meshheading:19213873-Adenosine Triphosphate, pubmed-meshheading:19213873-Animals, pubmed-meshheading:19213873-Carbenoxolone, pubmed-meshheading:19213873-Cell Dedifferentiation, pubmed-meshheading:19213873-Cells, Cultured, pubmed-meshheading:19213873-Connexins, pubmed-meshheading:19213873-Epithelial Cells, pubmed-meshheading:19213873-Flufenamic Acid, pubmed-meshheading:19213873-Gene Expression Regulation, pubmed-meshheading:19213873-Humans, pubmed-meshheading:19213873-Hypotonic Solutions, pubmed-meshheading:19213873-Macrophages, Alveolar, pubmed-meshheading:19213873-Mice, pubmed-meshheading:19213873-Mucociliary Clearance, pubmed-meshheading:19213873-Nerve Tissue Proteins, pubmed-meshheading:19213873-Osmotic Pressure, pubmed-meshheading:19213873-Paracrine Communication, pubmed-meshheading:19213873-Probenecid, pubmed-meshheading:19213873-RNA, Messenger, pubmed-meshheading:19213873-RNA Interference, pubmed-meshheading:19213873-Respiratory Mucosa, pubmed-meshheading:19213873-Stress, Physiological, pubmed-meshheading:19213873-Time Factors, pubmed-meshheading:19213873-Transfection, pubmed-meshheading:19213873-Xenopus
pubmed:year
2009
pubmed:articleTitle
Pannexin 1 contributes to ATP release in airway epithelia.
pubmed:affiliation
Division of Pulmonary and Critical Care Medicine (R-47), University of Miami Miller School of Medicine, 1600 NW 10th Ave., RMSB 7058, Miami, FL 33136, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural