Gene expression of tumor necrosis factor α and TNF-receptors, p55 and p75, in nonalcoholic steatohepatitis patients
Description
<jats:sec> <jats:title/> <jats:p>The main objective of this study was to analyze the pathogenic role of the tumor necrosis factor α (TNF-α) system in the development of nonalcoholic steatohepatitis (NASH). Fifty-two obese patients were studied. We investigated: (1) the expression of mRNA of TNF-α and their p55 and p75-receptors by quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) in hepatic and adipose tissues; and (2) the relationship between TNF-α, p55, and p75 and the severity of NASH. Obese patients without NASH were the control group. A remarkable increase in the expression of mRNA of TNF-α was found in patients with NASH in hepatic tissue (0.65 ± 0.54) and in peripheral fat (0.43 ± 0.45); in the control samples, the mRNA expression was 0.28 ± 0.32, <jats:italic toggle="yes">P</jats:italic> < .007, and 0.26 ± 0.22, <jats:italic toggle="yes">P</jats:italic> < .018, respectively. Furthermore, we found a significant increase in the mRNA levels of p55 receptor (2.42 ± 1.81 vs. 1.56 ± 1.17; <jats:italic toggle="yes">P</jats:italic> < .05); however, the mRNA expression of the p75 receptor was similar in both patients. Those patients with NASH with significant fibrosis presented an increase in the expression of mRNA TNF-α in comparison with those with a slight or nonexistent fibrosis. An overexpression of TNF-α mRNA is found in the liver and in the adipose tissue of NASH patients. The levels of mRNA-p55 are increased in the liver tissue of NASH patients. This overexpression is more elevated in patients with more advanced NASH. These findings suggest that the TNF-α system may be involved in the pathogenesis of NASH.</jats:p> </jats:sec>
Journal
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- Hepatology
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Hepatology 34 (6), 1158-1163, 2001-12
Ovid Technologies (Wolters Kluwer Health)
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Details 詳細情報について
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- CRID
- 1363107369068014720
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- NII Article ID
- 30015126099
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- ISSN
- 02709139
- https://id.crossref.org/issn/02709139
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- Data Source
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- Crossref
- CiNii Articles