Evidence map›Paper›PMID 24095726›Full record

ArticleFree radical biology & medicine2013

A functional link between heme oxygenase-1 and tristetraprolin in the anti-inflammatory effects of nicotine.

Md Jamal Uddin, Yeonsoo Joe, Min Zheng, Perry J Blackshear, Stefan W Ryter, Jeong Woo Park, Hun Taeg Chung

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Identification ofMolecules (Basel, Switzerland) · 2022
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. HO-1 overexpression and underexpression: Clinical implications.Archives of biochemistry and biophysics · 2019
    Review
  12. Article
  13. Pterostilbene 4'-Oxidative medicine and cellular longevity · 2018
    Article
  14. The role of RNA-binding protein tristetraprolin in cancer and immunity.Medical oncology (Northwood, London, England) · 2017
    Review
  15. Review
  16. Article
  17. Article
  18. 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 4 institutions in 3 countries.

Md Jamal UddinSchool of Biological Sciences, University of Ulsan, Ulsan 680-749, Korea.
Yeonsoo Joe
Min Zheng
Perry J Blackshear
Stefan W Ryter
Jeong Woo Park
Hun Taeg Chung
University of Ulsan · KRHarvard University · USNational Institute of Environmental Health Sciences · USYanbian University Hospital · CN

Funding

TTP and related proteins in the regulation of gene expressionZIAES090080 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BLACKSHEAR, PERRY J · 2009 to 2025
$52.6M
TTP AND RELATED PROTEINS IN INFLAMMATORY DISEASESZ01ES090080 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI BLACKSHEAR, PERRY J · 1998 to 2008
$5.3M
Intramural NIH HHS Z01 ES090080
6 · The paper itself

Abstract

Nicotine stimulates the cholinergic anti-inflammatory pathway and prevents excessive inflammation by inhibiting the release of inflammatory cytokines from macrophages. We have previously reported that heme oxygenase-1 (HO-1) and tristetraprolin (TTP) are induced by nicotine and mediate the anti-inflammatory function of nicotine in macrophages. However, it was not clear whether the two molecules are functionally linked. In this study, we sought to determine whether HO-1 associates with TTP to mediate the anti-inflammatory effects of nicotine. Inhibition of HO-1 activity or HO-1 expression attenuated the effects of nicotine on STAT3 activation, TTP induction, and TNF-α production in LPS-treated macrophages. Induction of HO-1 expression increased the level of TTP in the absence of nicotine. In an LPS-induced endotoxemia model, HO-1 deficiency blocked the effects of nicotine on the STAT3 phosphorylation, TTP induction, and LPS-induced TNF-α production in the liver. Downregulation of STAT3 by siRNA attenuated the effect of nicotine on TTP expression and TNF-α production but did not affect the nicotine-mediated induction of HO-1. In TTP knockout mice, nicotine treatment enhanced HO-1 expression and STAT3 activation but failed to inhibit LPS-induced TNF-α production. Our results suggest that HO-1 and TTP are functionally linked in mediating the anti-inflammatory effects of nicotine; HO-1 is necessary for the induction of TTP by nicotine. This novel nicotine-HO-1-TTP signaling pathway provides new possibilities for the treatment of inflammatory diseases.

Indexed as

AnimalsAnti-Inflammatory AgentsCell LineCell ProliferationCytokinesEndotoxemiaHeme Oxygenase-1InflammationLipopolysaccharidesLiverMacrophagesMiceMice, Inbred BALB CMice, KnockoutNicotinePhosphorylationAnti-Inflammatory AgentsCytokinesHeme Oxygenase-1LipopolysaccharidesNicotineRNA, Small InterferingStat3 protein, mouseSTAT3 Transcription FactorTristetraprolinTumor Necrosis Factor-alphaAnti-inflammatory effectscobalt protoporphyrinCoPPECLenhanced chemiluminescenceFree radicalsheme oxygenase-1HO-1knockoutKOlipopolysaccharideLPSNicotinesignal transducer and activator of transcription 3SnPPSTAT3tin protoporphyrinTNFtristetraprolinTTPtumor necrosis factorzinc protoporphyrinZnPP

Identifiers

PMID24095726
PMCPMC4798239
OpenAlexW2006281984

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.