Evidence map›Paper›PMID 22187147›Full record

ArticleAmino acids2012

Modulation of innate immune-related pathways in nicotine-treated SH-SY5Y cells.

Wen-Yan Cui, Ju Wang, Jinxue Wei, Junran Cao, Sulie L Chang, Jun Gu, Ming D Li

Open access · greenAbstract read
In one paragraph

Article in Amino acids, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Modulatory Effects of Nicotine on neuroHIV/neuroAIDS.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018
    Review
  6. Article
  7. Modulation Effect of HIV-1 Viral Proteins and Nicotine on Expression of the Immune-Related Genes in Brain of the HIV-1 Transgenic Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2016
    Article
  8. Article
  9. The HIV-1 transgenic rat model of neuroHIV.Brain, behavior, and immunity · 2015
    Review
  10. Article
  11. Article
  12. Gene expression and highly diluted molecules.Frontiers in pharmacology · 2014
    Article
  13. Article
  14. Article
  15. Article
  16. 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

7 authors at 3 institutions in 2 countries.

Wen-Yan CuiState Key Laboratory of Protein and Plant Gene Research, Peking University, Beijing, China.
Ju Wang
Jinxue Wei
Junran Cao
Sulie L Chang
Jun Gu
Ming D Li
University of Virginia · USPeking University · CNSeton Hall University · US

Funding

GENE EXPRESSION PROFILING DURING EXPOSURE TO NICOTINER01DA013783 · NIDA · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI LI, MING D · 2000 to 2008
$3.9M
Mechanisms of Nicotine's Behavioral Effects on the HIV-1 Transgenic RatR01DA026356 · NIDA · SETON HALL UNIVERSITY · PI CHANG, SULIE L., LI, MING D · 2009 to 2014
$2.4M
Morphine Actions on the Immune SystemK02DA016149 · NIDA · SETON HALL UNIVERSITY · PI CHANG, SULIE L. · 2003 to 2012
$1.1M
NIDA NIH HHS DA-013783NIDA NIH HHS DA-016149NIDA NIH HHS DA-026356NIDA NIH HHS K02 DA016149NIDA NIH HHS R01 DA013783NIDA NIH HHS R01 DA026356
6 · The paper itself

Abstract

Although nicotine has a broad impact on both the central and peripheral nervous systems, the molecular mechanisms remain largely unknown, especially at the signaling pathway level. To investigate that aspect, we employed both conventional molecular techniques, such as quantitative real-time PCR and Western blotting analysis, and high-throughput microarray approach to identify the genes and signaling pathways that are modulated by nicotine. We found 14 pathways significantly altered in SH-SY5Y neuroblastoma cells. Of these, the Toll-like receptor pathway (TLR; p = 2.57 × 10(-4)) is one of the most important innate immune pathways. The death receptor pathway (DR; p = 8.71 × 10(-4)), whose transducers coordinate TLR signals and help conduct the host immune response to infection, was also significantly changed by nicotine. Furthermore, we found that several downstream pathways of TLR and DR signaling, such as PI3K/AKT signaling (p = 9.55 × 10(-6)), p38 signaling (p = 2.40 × 10(-6)), and ERK signaling (p = 1.70 × 10(-4)), were also significantly modulated by nicotine. Interestingly, most of the differentially expressed genes in these pathways leading to nuclear factor κB (NF-κB) activation and those important inhibitors of pathways leading to apoptosis, including FLIP and Bcl-2, were up-regulated by nicotine. Taken together, our findings demonstrate that nicotine can regulate multiple innate immune-related pathways, and our data thus provide new clues to the molecular mechanisms underlying nicotine's regulatory effects on neurons.

Indexed as

ApoptosisCell LineDose-Response Relationship, DrugGene ExpressionGene Expression RegulationHumansImmunity, InnateImmunologic FactorsMAP Kinase Signaling SystemNeuronsNF-kappa BNicotineOligonucleotide Array Sequence AnalysisReceptors, Death DomainToll-Like ReceptorsTranscriptomeImmunologic FactorsNF-kappa BNicotineReceptors, Death DomainToll-Like Receptors

Identifiers

PMID22187147
PMCPMC5574163
OpenAlexW2035889212

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.