Linked Life Data

16158611

Source:http://linkedlifedata.com/resource/pubmed/id/16158611

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
31
pubmed:dateCreated
2005-9-14
pubmed:abstractText
Engagement of T cell receptors by antigen-presenting cells or stimulation by cytokines determine whether the cell will become activated, anergic or die via apoptosis or necrosis. Ca2+ is a key second messenger that delivers signal from the cell surface, reactive oxygen intermediates and nitric oxide are recently recognized as important mediators of T cell activation. Nitric oxide is a multifunctional intracellular and intercellular messenger induces mitochondrial biogenesis in many cell types, such as lymphocytes. Mitochondria produce reactive oxygen intermediates and store and release Ca2+ in response to activation and death signals. Rapid Ca2+ fluxing is increased while sustained Ca2+ signaling is decreased in lupus T cells. Lupus T cells contain increased numbers and mass of mitochondria. Serum nitric oxide levels and production of nitric oxide by monocytes is increased in patients with systemic lupus erythematosus. Lupus T cells exhibit mitochondrial hyperpolarization and increased mitochondrial mass, which confer predisposition to necrosis rather than apoptosis in response to repetitive activation and death signals. Exposure of normal T cells to nitric oxide dose-dependently increase the mitochondrial mass and mimic rapid and sustained Ca2+ signal abnormalities observed in lupus T cells. Thus increased mitochondrial biogenesis may account for altered Ca2+ handling and represents novel targets for pharmacological intervention in SLE.
pubmed:language
hun
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0030-6002
pubmed:author
pubmed:issnType
Print
pubmed:day
31
pubmed:volume
146
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1625-30
pubmed:dateRevised
2009-10-21
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
[Signal transduction abnormalities in systemic lupus erythematosus].
pubmed:affiliation
Semmelweis Egyetem, Altalános Orvostudományi Kar, 111. Belgyógyászati Klinika Reumatológiai es Fizioterápiás Tanszéki Csoport, I. Részleg, Budai Irgalmasrendi Kórház, Budapest.
pubmed:publicationType
Journal Article, English Abstract, Review