Source:http://linkedlifedata.com/resource/pubmed/id/12471144
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
12
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| pubmed:dateCreated |
2002-12-9
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| pubmed:abstractText |
Cytokine-induced lung expression of the endothelial cell (EC) leukocyte receptor P-selectin initiates leukocyte rolling. To understand the early EC signaling that induces the expression, we conducted real-time digital imaging studies in lung venular capillaries. To compare receptor- vs nonreceptor-mediated effects, we infused capillaries with respectively, TNF-alpha and arachidonate. At concentrations adjusted to give equipotent increases in the cytosolic Ca(2+), both agents increased reactive oxygen species (ROS) production and EC P-selectin expression. Blocking the cytosolic Ca(2+) increases abolished ROS production; blocking ROS production abrogated P-selectin expression. TNF-alpha, but not arachidonate, released Ca(2+) from endoplasmic stores and increased mitochondrial Ca(2+). Furthermore, Ca(2+) depletion abrogated TNF-alpha responses partially, but arachidonate responses completely. These differences in Ca(2+) mobilization by TNF-alpha and arachidonate were reflected in spatial patterning in the capillary in that the TNF-alpha effects were localized at branch points, while the arachidonate effects were nonlocalized and extensive. Furthermore, mitochondrial blockers inhibited the TNF-alpha- but not the arachidonate-induced responses. These findings indicate that the different modes of Ca(2+) mobilization determined the spatial patterning of the proinflammatory response in lung capillaries. Responses to TNF-alpha revealed that EC mitochondria regulate the proinflammatory process by generating ROS that activate P-selectin expression.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Aldehydes,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Fluoresceins,
http://linkedlifedata.com/resource/pubmed/chemical/Fluorescent Dyes,
http://linkedlifedata.com/resource/pubmed/chemical/Heterocyclic Compounds, 3-Ring,
http://linkedlifedata.com/resource/pubmed/chemical/P-Selectin,
http://linkedlifedata.com/resource/pubmed/chemical/Reactive Oxygen Species,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/Xanthenes,
http://linkedlifedata.com/resource/pubmed/chemical/diacetyldichlorofluorescein,
http://linkedlifedata.com/resource/pubmed/chemical/mitotracker green FM,
http://linkedlifedata.com/resource/pubmed/chemical/mitotracker orange,
http://linkedlifedata.com/resource/pubmed/chemical/rhod-2
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| pubmed:status |
MEDLINE
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| pubmed:month |
Dec
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
15
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| pubmed:volume |
169
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
7078-86
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:12471144-Aldehydes,
pubmed-meshheading:12471144-Animals,
pubmed-meshheading:12471144-Calcium,
pubmed-meshheading:12471144-Calcium Signaling,
pubmed-meshheading:12471144-Capillaries,
pubmed-meshheading:12471144-Endothelium, Vascular,
pubmed-meshheading:12471144-Fluoresceins,
pubmed-meshheading:12471144-Fluorescent Dyes,
pubmed-meshheading:12471144-Heterocyclic Compounds, 3-Ring,
pubmed-meshheading:12471144-Inflammation,
pubmed-meshheading:12471144-Lung,
pubmed-meshheading:12471144-Male,
pubmed-meshheading:12471144-Microscopy, Confocal,
pubmed-meshheading:12471144-Mitochondria,
pubmed-meshheading:12471144-P-Selectin,
pubmed-meshheading:12471144-Rats,
pubmed-meshheading:12471144-Rats, Sprague-Dawley,
pubmed-meshheading:12471144-Reactive Oxygen Species,
pubmed-meshheading:12471144-Tumor Necrosis Factor-alpha,
pubmed-meshheading:12471144-Veins,
pubmed-meshheading:12471144-Xanthenes
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| pubmed:year |
2002
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| pubmed:articleTitle |
Mitochondrial reactive oxygen species regulate spatial profile of proinflammatory responses in lung venular capillaries.
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| pubmed:affiliation |
St. Luke's-Roosevelt Hospital Center, Department of Physiology and Cellular Biophysics, College of Physicians and Surgeons, Columbia University, New York, NY 10019, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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