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Gene expression of tumor necrosis factor α and TNF-receptors, p55 and p75, in nonalcoholic steatohepatitis patients
Abstract
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, P < .007, and 0.26 ± 0.22, P < .018, respectively. Furthermore, we found a significant increase in the mRNA levels of p55 receptor (2.42 ± 1.81 vs. 1.56 ± 1.17; P < .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.
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Metadata
- Authors
- Crespo, J., Cayón, A., Fernández-Gil, P., Hernández-Guerra, M., Mayorga, M., Domínguez-Díez, A., Fernández-Escalante, J. C., & Pons-Romero, F.
- Venue
- Hepatology
- Published
- 2001-12
- Volume
- 34
- Issue
- 6
- Pages
- 1158-1163
- ISSN
- 0270-9139 (ISSN-L)
- OpenAlex
- W2027391841
- Cited by
- 693
- References
- 3
- FWCI
- 10.70
- Type
- journal article
- Language
- en
- Open access
- closed
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