Ethanol induces the production of cytokines via the Ca2+, MAP kinase, HIF-1α, and NF-κB pathway

Jeong, Hyun‐Ja; Hong, Seung‐Heon; Park, Raekil; An, Nyeon‐Hyoung

doi:10.1016/j.lfs.2005.04.014

Cited by 25 publications

(14 citation statements)

References 46 publications

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“…These findings are consistent with a pro-tumorigenic role for mMCP6 + (tryptase+) mast cells [49], especially in the stroma where invasion occurs in CRC [28]. Our group (and others) previously showed that alcohol stimulates the expression of tryptase in mast cells [11,50]—an effect that is exacerbated by circadian disruption in our study—through as of yet unknown mechanisms. Several studies have shown the deleterious effect of circadian disruption (and particularly LD shifting) on the gut microbiota [51], and the microbiota could impact intestinal inflammation including mast cell phenotype, and consequently impact carcinogenesis [52].…”

Section: Discussionsupporting

confidence: 91%

Light/Dark Shifting Promotes Alcohol-Induced Colon Carcinogenesis: Possible Role of Intestinal Inflammatory Milieu and Microbiota

Bishehsari

Saadalla

Khazaie

et al. 2016

IJMS

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Background: Colorectal cancer (CRC) is associated with the modern lifestyle. Chronic alcohol consumption—a frequent habit of majority of modern societies—increases the risk of CRC. Our group showed that chronic alcohol consumption increases polyposis in a mouse mode of CRC. Here we assess the effect of circadian disruption—another modern life style habit—in promoting alcohol-associated CRC. Method: TS4Cre × adenomatous polyposis coli (APC)lox468 mice underwent (a) an alcohol-containing diet while maintained on a normal 12 h light:12 h dark cycle; or (b) an alcohol-containing diet in conjunction with circadian disruption by once-weekly 12 h phase reversals of the light:dark (LD) cycle. Mice were sacrificed after eight weeks of full alcohol and/or LD shift to collect intestine samples. Tumor number, size, and histologic grades were compared between animal groups. Mast cell protease 2 (MCP2) and 6 (MCP6) histology score were analyzed and compared. Stool collected at baseline and after four weeks of experimental manipulations was used for microbiota analysis. Results: The combination of alcohol and LD shifting accelerated intestinal polyposis, with a significant increase in polyp size, and caused advanced neoplasia. Consistent with a pathogenic role of stromal tryptase-positive mast cells in colon carcinogenesis, the ratio of mMCP6 (stromal)/mMCP2 (intraepithelial) mast cells increased upon LD shifting. Baseline microbiota was similar between groups, and experimental manipulations resulted in a significant difference in the microbiota composition between groups. Conclusions: Circadian disruption by Light:dark shifting exacerbates alcohol-induced polyposis and CRC. Effect of circadian disruption could, at least partly, be mediated by promoting a pro-tumorigenic inflammatory milieu via changes in microbiota.

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Section: Discussionsupporting

confidence: 91%

Light/Dark Shifting Promotes Alcohol-Induced Colon Carcinogenesis: Possible Role of Intestinal Inflammatory Milieu and Microbiota

Bishehsari

Saadalla

Khazaie

et al. 2016

IJMS

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“…Pharmacological research has suggested that MAPK is a central pathway involved in Nrf2 activation and translocation for highly specialized protein synthesis, including most readily inducible HO-1 [35][36][37]. Our results showed that the p38 and ERK signaling transduction pathway participated in the Nrf2 translocation from cytoplasm into nucleus and HO-1 induction by quercetin and ethanol, which is analogous to the findings in diallyl sulfide-treated HepG2 [38] and ethanol-treated HMC-1 cells [39]. Furthermore, the ERK pathway is mainly responsible for quercetin-derived HO-1 induction while p38 is mainly responsible for ethanol-stimulated HO-1 induction.…”

Section: Discussionsupporting

confidence: 85%

Quercetin protects human hepatocytes from ethanol-derived oxidative stress by inducing heme oxygenase-1 via the MAPK/Nrf2 pathways

Yao

Nüssler

Liu

et al. 2007

Journal of Hepatology

336

178

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“…Using the WEBGESTALT search engine, which queries different databases, including KEGG, BioCarta, and GO (Gene Ontology) (18)(19)(20), functional group analysis revealed that kinase and signaling pathways were overrepresented in genes divergent between alcohol-preferring and nonpreferring genotypes. The result supports previous suggestions that the mitogen-activated protein kinase, NF-B, and IL-6 signaling pathways (and CREBBP) are sensitive to alcohol (21). Known functional interactions (summarized in Fig.…”

Section: Meta-analysis Identifies Candidate Genes For High and Low Amsupporting

confidence: 89%

Toward understanding the genetics of alcohol drinking through transcriptome meta-analysis

Mulligan

Ponomarev

Hitzemann

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

325

378

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Much evidence from studies in humans and animals supports the hypothesis that alcohol addiction is a complex disease with both hereditary and environmental influences. Molecular determinants of excessive alcohol consumption are difficult to study in humans. However, several rodent models show a high or low degree of alcohol preference, which provides a unique opportunity to approach the molecular complexities underlying the genetic predisposition to drink alcohol. Microarray analyses of brain gene expression in three selected lines, and six isogenic strains of mice known to differ markedly in voluntary alcohol consumption provided >4.5 million data points for a meta-analysis. A total of 107 arrays were obtained and arranged into six experimental data sets, allowing the identification of 3,800 unique genes significantly and consistently changed between all models of high or low amounts of alcohol consumption. Several functional groups, including mitogen-activated protein kinase signaling and transcription regulation pathways, were found to be significantly overrepresented and may play an important role in establishing a high level of voluntary alcohol drinking in these mouse models. Data from the general meta-analysis was further filtered by a congenic strain microarray set, from which cis-regulated candidate genes for an alcohol preference quantitative trait locus on chromosome 9 were identified: Arhgef12, Carm1, Cryab, Cox5a, Dlat, Fxyd6, Limd1, Nicn1, Nmnat3, Pknox2, Rbp1, Sc5d, Scn4b, Tcf12, Vps11, and Zfp291 and four ESTs. The present study demonstrates the use of (i) a microarray meta-analysis to analyze a behavioral phenotype (in this case, alcohol preference) and (ii) a congenic strain for identification of cis regulation.alcoholism ͉ gene expression ͉ microarray

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Ethanol induces the production of cytokines via the Ca2+, MAP kinase, HIF-1α, and NF-κB pathway

Cited by 25 publications

References 46 publications

Light/Dark Shifting Promotes Alcohol-Induced Colon Carcinogenesis: Possible Role of Intestinal Inflammatory Milieu and Microbiota

Light/Dark Shifting Promotes Alcohol-Induced Colon Carcinogenesis: Possible Role of Intestinal Inflammatory Milieu and Microbiota

Quercetin protects human hepatocytes from ethanol-derived oxidative stress by inducing heme oxygenase-1 via the MAPK/Nrf2 pathways

Toward understanding the genetics of alcohol drinking through transcriptome meta-analysis

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