Linked Life Data

17085430

Source:http://linkedlifedata.com/resource/pubmed/id/17085430

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2006-11-6
pubmed:abstractText
Phenotypic heterogeneity in pulmonary vascular endothelial cells extends to regulation of endothelial permeability, a process which often depends upon Ca2 + entry from the extracellular space. Scanning electron microscopy of vascular corrosion casts has documented distinct patterns of barrier disruption. Store depletion and activation of Ca2 + entry via canonical transient potential channels (TRPC1 and TRPC4) disrupts the barrier in extraalveolar vessels. In contrast, numerous other models of acute lung injury, including high vascular pressure- or epoxyeicosatrienoic acid-induced injury, specifically disrupt the alveolar septal barrier. This review discusses Ca2 + permeant channels which potentially could be involved in regulation of barrier integrity in the alveolar septal compartment: transient receptor potential channels, cyclic nucleotide gated channels, purinergic (P2X) channels, and T-type voltage gated channels. The evidence for the vanilloid transient receptor potential channel TRPV4 in regulating septal barrier function is discussed. Adaptations in barrier function in chronic pulmonary hypertension are reviewed, notably the loss of a store depletion-dependent permeability response in the intact lung. Finally, the authors propose that since specific disruption of the alveolar septal barrier will have deleterious functional consequences, such as alveolar flooding and impairment of gas exchange, identification of specific molecular targets for Ca2 + entry-dependent regulation of barrier function in this compartment is needed.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1073-9688
pubmed:author
pubmed:issnType
Print
pubmed:volume
13
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
725-39
pubmed:dateRevised
2007-12-3
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Ca2+ channels and pulmonary endothelial permeability: insights from study of intact lung and chronic pulmonary hypertension.
pubmed:affiliation
Department of Physiology and the Center for Lung Biology, University of South Alabama, Mobile, Alabama 36688, USA. mtownsley@usouthal.edu
pubmed:publicationType
Journal Article, Comparative Study, Review, Research Support, N.I.H., Extramural