Linked Life Data

11050060

Source:http://linkedlifedata.com/resource/pubmed/id/11050060

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2000-11-13
pubmed:abstractText
As a part of the defense mechanism of the host to viral infection, interferons induce the transcription of several genes. These interferon-inducible genes contribute to the eradication of the viruses. Whereas some studies suggested the participation of a dsRNA-dependent protein kinase in the host reaction to hepatitis C virus infection, the involvement of other interferon-inducible genes has not been evaluated. Furthermore, there has been no analysis on the expression profile of multiple interferon-inducible genes. The aim of this study was to clarify the hepatic mRNA expression profile of interferon-inducible genes with a special concern to chronic hepatitis C. A total of 76 liver biopsy samples (28 with chronic hepatitis C, 10 with chronic hepatitis B, 9 with alcoholic liver disease, 14 with autoimmune hepatitis, 10 with primary biliary cirrhosis, and 5 of normal liver) were enrolled. The expression of the following genes was quantified by competitive reverse transcription-polymerase chain reaction and was compared according to the etiology; dsRNA-dependent protein kinase (PKR), 2',5'-oligoadenylate synthetase (2,5-AS), latent cellular endoribonuclease (RNase L), RNase L inhibitor, and MxA. As a result, PKR mRNA was significantly overexpressed in the liver of chronic hepatitis C compared with those of other etiologies (P =.0178), and it correlated significantly with serum alanine transaminase values (r =.51, P =.0054). Also, the expression of the RNase L inhibitor showed a significant reduction in chronic hepatitis C (P =.0184). The expressions of 2,5-AS, RNase L, and MxA were not different significantly irrespective to the etiology. In conclusion, hepatic overexpression of PKR and reduced expression of RNase L inhibitor seem to contribute to the anti-HCV mechanism characteristically.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0270-9139
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1089-95
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11050060-ATP-Binding Cassette Transporters, pubmed-meshheading:11050060-Adult, pubmed-meshheading:11050060-Aged, pubmed-meshheading:11050060-Antiviral Agents, pubmed-meshheading:11050060-Chaperonins, pubmed-meshheading:11050060-Female, pubmed-meshheading:11050060-Gene Expression Regulation, pubmed-meshheading:11050060-Hepatitis C, Chronic, pubmed-meshheading:11050060-Humans, pubmed-meshheading:11050060-Interferons, pubmed-meshheading:11050060-Liver, pubmed-meshheading:11050060-Liver Diseases, pubmed-meshheading:11050060-Male, pubmed-meshheading:11050060-Middle Aged, pubmed-meshheading:11050060-Protein Kinases, pubmed-meshheading:11050060-Proteins, pubmed-meshheading:11050060-RNA, Double-Stranded, pubmed-meshheading:11050060-RNA, Messenger, pubmed-meshheading:11050060-Suppression, Genetic, pubmed-meshheading:11050060-Virus Diseases, pubmed-meshheading:11050060-eIF-2 Kinase
pubmed:year
2000
pubmed:articleTitle
Intrahepatic mRNA expression of interferon-inducible antiviral genes in liver diseases: dsRNA-dependent protein kinase overexpression and RNase L inhibitor suppression in chronic hepatitis C.
pubmed:affiliation
Second Department of Internal Medicine, Tokyo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't