Evidence map›Paper›PMID 30876690›Full record

ArticleBiochemical and biophysical research communications2019

Suppressed hepatocyte proliferation via a ROS-HNE-P21 pathway is associated with nicotine- and cotinine-enhanced alcoholic fatty liver in mice.

Xue Chen, Kesheng Wang, Arthur I Cederbaum, Yongke Lu

Open access · greenAbstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 32% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 8 citations in OpenAlex.

  1. Review
  2. Cigarette smoking and alcohol-related liver disease.Liver research (Beijing, China) · 2024
    Review
  3. Article
  4. Article
  5. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Xue ChenDepartment of Health Sciences, College of Public Health, East Tennessee State University, Johnson City, TN, 37614, USA.
Kesheng WangDepartment of Biostatistics and Epidemiology, College of Public Health, East Tennessee State University, Johnson City, TN, 37614, USA.
Arthur I CederbaumDepartment of Pharmacological Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, 10029, USA.
Yongke LuDepartment of Health Sciences, College of Public Health, East Tennessee State University, Johnson City, TN, 37614, USA. Electronic address: luy004@etsu.edu.
East Tennessee State University · USIcahn School of Medicine at Mount Sinai · US

Funding

Nicotine and Alcoholic Liver DiseaseR01AA024723 · NIAAA · MARSHALL UNIVERSITY · PI LU, YONGKE · 2016 to 2020
$1.8M
CYP2A5 and alcoholic liver diseaseR21AA020877 · NIAAA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LU, YONGKE · 2013 to 2014
$438k
NIAAA NIH HHS R01 AA024723NIAAA NIH HHS R21 AA020877
6 · The paper itself

Abstract

CYP2A5 is a major enzyme responsible for nicotine and cotinine metabolism in mice. Nicotine and cotinine enhance alcoholic fatty liver in wild type (WT) mice but not in CYP2A5 knockout (KO) mice, and reactive oxygen species (ROS) generated during the CYP2A5-mediated metabolism contributes to the enhancing effect. In combination with ethanol, nicotine and cotinine increased lipid peroxidation end product 4-hydroxynonenal (HNE) in WT mice but not in KO mice. In ethanol-fed KO mice, only 5 and 10 genes were regulated by nicotine and cotinine, respectively. However, in ethanol-fed WT mice, 59 and 104 genes were regulated by nicotine and cotinine, respectively, and 7 genes were up-regulated by both nicotine and cotinine. Plin 2 and Cdkn1a are among the 7 genes. Plin2 encodes adipose differentiation-related protein (ADRP), a lipid droplet-associated protein, which was confirmed to be increased by nicotine and cotinine in WT mice but not in KO mice. Cdkn1a encodes P21 and elevated P21 in nuclei was also confirmed. HNE can increase P21 and P21 inhibit cell proliferation. Consistently, hepatocyte proliferation markers proliferating cell nuclear antigen (PCNA) and Ki67 were decreased in WT mice but not in KO mice by nicotine/ethanol and cotinine/ethanol, respectively. These results suggest that inhibition of liver proliferation via a ROS-HNE-P21 pathway is involved in nicotine- and cotinine-enhanced alcoholic fatty liver.

Indexed as

AldehydesAnimalsAryl Hydrocarbon HydroxylasesCell ProliferationCotinineCyclin-Dependent Kinase Inhibitor p21Cytochrome P450 Family 2Disease Models, AnimalFatty Liver, AlcoholicFemaleHepatocytesLiver RegenerationMiceMice, KnockoutNicotinePerilipin-24-hydroxy-2-nonenalAldehydesAryl Hydrocarbon HydroxylasesCdkn1a protein, mouseCotinineCyclin-Dependent Kinase Inhibitor p21Cyp2a5 protein, mouseCytochrome P450 Family 2NicotinePerilipin-2Plin2 protein, mouseReactive Oxygen SpeciesCYP2A5HNEKi67P21PCNAPlin2ROS

Identifiers

PMID30876690
PMCPMC6433518
OpenAlexW2921147898

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.