Linked Life Data

17909849

Source:http://linkedlifedata.com/resource/pubmed/id/17909849

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2008-1-24
pubmed:abstractText
Generally, a formation of paracellular gaps is considered to be the main pathway for fluid passage across endothelia. A model substance for studies in vitro is the vasodilatory peptide bradykinin, which has important functions in inflammation and vascular fluid balance. The mechanisms by which it increases endothelial permeability are not as yet clearly defined. Paracellular gap formation was approached using atomic force microscopy (AFM) on human umbilical vein endothelial cells grown on permeable filter supports. To further distinguish between para- vs transcellular fluid passage, a standard permeability assay was modified by a rapid cooling protocol to specifically inhibit vesicular transport pathways. Cell layers stimulated with bradykinin (1 microM) did not show significant alterations at the cellular junctions. However, gap formation was easily detectable by AFM after addition of the Ca(2+)-ionophore ionomycin (1 microM), which was taken as a positive control for cellular contraction. At 37 degrees C, bradykinin enhanced fluorescein isothiocyanate-dextran permeability by 48 +/- 11%. This was blocked by rapid cooling of the sample, indicating a vesicular mechanism of fluid transport. Contrastingly, ionomycin-induced permeability (259 +/- 43%) persisted after cooling (230 +/- 44%), thereby confirming paracellular gap formation. Accordingly, endocytotic vesicle formation, as detected by fluorescence microscopy, was upregulated by 68 +/- 15% through bradykinin action, while ionomycin did not show a significant effect (7 +/- 26%). The combined results of both permeability and morphometric studies lead to the conclusion that bradykinin promotes transcellular fluid passage rather than increasing paracellular diffusion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0031-6768
pubmed:author
pubmed:issnType
Print
pubmed:volume
455
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1007-16
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Bradykinin does not induce gap formation between human endothelial cells.
pubmed:affiliation
Institute of Physiology II, University of Münster, Robert-Koch-Str. 27b, 48149 Münster, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't