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Cited by 179Alcohol Consumption and Health EffectsCell death mechanisms and regulationLiver physiology and pathology

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Elevated interleukin-6 during ethanol consumption acts as a potential endogenous protective cytokine against ethanol-induced apoptosis in the liver: involvement of induction of Bcl-2 and Bcl-xL proteins

Hong, Feng, Kim, Won-Ho, Tian, Zhigang, Jaruga, Barbara, Ishac, Edward, Shen, Xuening, Gao, Bin·2002·Oncogene
DOI 10.1038/sj.onc.1205016
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Abstract

Elevation of serum interleukin-6 (IL-6) levels is always associated with alcoholic liver disease (ALD), but the significance of such elevation is not clear. Here we show that chronic ethanol consumption induces significant apoptosis in the liver of IL-6 (-/-) mice but not IL-6 (+/+) mice. IL-6 (-/-) hepatocytes are more susceptible to ethanol- and tumor necrosis factor alpha- (TNFalpha-) induced apoptotic killing, which can be corrected by IL-6. Expression of both anti-apoptotic (such as Bcl-2 and Bcl-x(L)) and proapoptotic (such as Bax) proteins is markedly elevated in the liver of human ALD and chronically ethanol-fed IL-6 (+/+) mice. On the contrary, induction of Bcl-2 and Bcl-x(L) is not observed in the liver of chronically ethanol-fed IL-6 (-/-) mice, whereas expression of Bax protein remains elevated. Injection of IL-6 markedly induces expression of Bcl-2 and Bcl-x(L) but not Bax in the liver. Finally, high concentrations of ethanol inhibit IL-6-activated anti-apoptotic signal, but increasing the concentrations of IL-6 is able to overcome such inhibitory effect. These findings suggest that elevated serum IL-6 levels in ALD may overcome the inhibitory effect of ethanol on IL-6-mediated anti-apoptotic signals and prevent alcohol-induced hepatic apoptosis by induction of Bcl-2 and Bcl-x(L).

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Metadata

Authors
Hong, F., Kim, W.-H., Tian, Z., Jaruga, B., Ishac, E., Shen, X., & Gao, B.
Affiliations
  • National Institutes of Health (US)
  • University of Science and Technology of China (CN)
  • Virginia Commonwealth University (US)
Corresponding author
Gao, Bin
ORCID
Venue
Oncogene
Publisher
Springer Science and Business Media LLC
Published
2002-01-03
Volume
21
Issue
1
Pages
32-43
ISSN
  • 0950-9232 (ISSN-L)
  • 1476-5594
DOI
10.1038/sj.onc.1205016
OpenAlex
W2057210516
Cited by
179
References
0
Citations by year
2026: 2 · 2025: 4 · 2024: 5 · 2023: 4 · 2022: 4 · 2021: 8 · 2020: 10 · 2019: 7 · 2018: 7 · 2017: 10 · 2016: 8 · 2015: 6 · 2014: 6 · 2013: 7 · 2012: 11
FWCI
7.68
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Oncogene (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01aa012637-03)
  • National Institute on Alcohol Abuse and Alcoholism (R01 AA 12637)
Topics
  • Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Health Sciences › Medicine › Hepatology › Liver physiology and pathology
Keywords
interleukin-6, ethanol consumption, alcoholic liver disease, hepatocyte apoptosis, Bcl-2, Bcl-xL, Bax, TNF-α, anti-apoptotic signaling, IL-6 knockout mice
MeSH terms
Ethanol, Alcoholism, Animals, Body Weight, Cells, Cultured, Gene Expression Regulation, Genotype, Humans, Liver, Liver Diseases, Alcoholic, Male, Organ Size, Tumor Necrosis Factor-alpha, Interleukin-6, Apoptosis, Mice, Knockout, Proto-Oncogene Proteins c-bcl-2, Genes, bcl-2, Genetic Predisposition to Disease, Hepatocytes, bcl-X Protein, Mice

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