Source:http://linkedlifedata.com/resource/pubmed/id/16309569
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
|
pubmed:dateCreated |
2005-11-28
|
pubmed:abstractText |
Heme oxygenase (HO)-1, the inducible isoform of the rate-limiting enzyme of heme degradation, and peroxiredoxin (Prx) I, a thioredoxin-dependent peroxidase, are multifunctional antioxidant stress proteins which are coordinately up-regulated by oxidative stress in cell cultures. HO-1 and Prx I exhibit a different hepatic cellular and subcellular localization. Here, a distinct expression pattern of the two genes was confirmed by in situ hybridization of normal rat liver. Moreover, expression of the HO-1 and Prx I genes was determined in a model of acutely damaged rat liver which was elicited by application of a single dose of carbon tetrachloride (CCl4). The mRNA levels of the HO-1 and Prx I genes were induced in whole livers of CCl4-treated rats with differential kinetics as determined by Northern blot analysis. While HO-1 mRNA was induced up to 48 hr, Prx I exhibited a maximum level of mRNA after 12 hr of treatment with CCl4. CCl4-dependent oxidative stress led to a focal increase of perivenous HO-1 positive liver cells with simultaneous loss of Prx I immunoreactivity. Taken together, the complementary hepatic gene expression pattern of HO-1 and Prx I in response to oxidative stress may suggest a functional interplay of these antioxidant genes.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Carbon Tetrachloride,
http://linkedlifedata.com/resource/pubmed/chemical/Heme Oxygenase-1,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxidases,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxiredoxins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger
|
pubmed:status |
MEDLINE
|
pubmed:month |
Oct
|
pubmed:issn |
1165-158X
|
pubmed:author | |
pubmed:issnType |
Electronic
|
pubmed:day |
3
|
pubmed:volume |
51
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
471-7
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:16309569-Animals,
pubmed-meshheading:16309569-Carbon Tetrachloride,
pubmed-meshheading:16309569-Disease Models, Animal,
pubmed-meshheading:16309569-Gene Expression Regulation, Enzymologic,
pubmed-meshheading:16309569-Heme Oxygenase-1,
pubmed-meshheading:16309569-Kinetics,
pubmed-meshheading:16309569-Liver,
pubmed-meshheading:16309569-Male,
pubmed-meshheading:16309569-Oxidative Stress,
pubmed-meshheading:16309569-Peroxidases,
pubmed-meshheading:16309569-Peroxiredoxins,
pubmed-meshheading:16309569-RNA, Messenger,
pubmed-meshheading:16309569-Rats,
pubmed-meshheading:16309569-Rats, Wistar
|
pubmed:year |
2005
|
pubmed:articleTitle |
Complementary regulation of heme oxygenase-1 and peroxiredoxin I gene expression by oxidative stress in the liver.
|
pubmed:affiliation |
Institute for Clinical Immunology und Transfusion Medicine, University of Giessen Langhansstr. 7, 35392 Giessen, Germany. Stephan.Immenschuh@immunologie.med.uni-giessen.de
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|