Linked Life Data

12230868

Source:http://linkedlifedata.com/resource/pubmed/id/12230868

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2002-9-16
pubmed:abstractText
Heme oxygenase (HO) enzymes catalyze the initial reaction in heme catabolism. HO-1 is an inducible isoform that is up-regulated by diverse stimuli, including inflammatory cytokines and factors that promote oxidative stress. HO-1 is a cytoprotective enzyme that degrades heme, a potent oxidant, to generate carbon monoxide, biliverdin (subsequently reduced to bilirubin), and iron. Recently, we found that thioredoxin (TRX), a disulfide reductase enzyme known to be important for the binding of transcription factors to DNA, contributes to the induction of HO-1 by inflammatory mediators. In the present study, we extended this observation and determined that, similar to HO-1, TRX and TRX reductase (TR) are induced by bacterial lipopolysaccharide in macrophages at the level of mRNA and protein. However, maximal induction of TRX and TR precedes that of HO-1. Increased expression of HO-1 in the cytoplasm of inflammatory cells corresponds to a translocation of TRX into the nucleus of these cells. Finally, transfection of TRX into macrophages promoted an increase in HO-1 protein. Taken together, these data support the concept that the TRX system contributes to the up-regulation of HO-1 under conditions associated with increased oxidative stress.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1523-0864
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
569-75
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2002
pubmed:articleTitle
Modulation of the thioredoxin system during inflammatory responses and its effect on heme oxygenase-1 expression.
pubmed:affiliation
Pulmonary and Critical Care, Brigham and Women's Hospital, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't