Evidence map›Paper›PMID 21339300›Full record

ArticleThe Journal of biological chemistry2011

Tristetraprolin-dependent post-transcriptional regulation of inflammatory cytokine mRNA expression by apolipoprotein A-I: role of ATP-binding membrane cassette transporter A1 and signal transducer and activator of transcription 3.

Kai Yin, Xiang Deng, Zhong-Cheng Mo, Guo-Jun Zhao, Jin Jiang, Li-Bao Cui, Chun-Zhi Tan, Ge-Bo Wen, Yuchang Fu, Chao-Ke Tang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Apolipoprotein A (ApoA) in Neurological Disorders: Connections and Insights.International journal of molecular sciences · 2025
    Review
  6. Review
  7. High-Density Lipoproteins in Non-Cardiovascular Diseases.International journal of molecular sciences · 2022
    Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. AIBP, inflammation, and atherosclerosis.Journal of lipid research · 2018
    Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Changes in serum inflammatory markers are associated with changes in apolipoprotein A1 but not B after the initiation of dialysis.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2014
    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

10 authors at 4 institutions in 3 countries.

Kai YinInstitute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, Life Science Research Center, University of South China, Hengyang, 421001, China.
Xiang Deng
Zhong-Cheng Mo
Guo-Jun Zhao
Jin Jiang
Li-Bao Cui
Chun-Zhi Tan
Ge-Bo Wen
Yuchang Fu
Chao-Ke Tang
Institute for Atherosclerosis Research · RUFirst Affiliated Hospital of University of South China · CNUniversity of Alabama at Birmingham · USUniversity of South China · CN

Funding

CSRD VA I01 CX002010
6 · The paper itself

Abstract

Atherosclerosis is an inflammatory disease characterized by the accumulation of macrophages in the arterial intima. The activated macrophages secreted more pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α, which promote the development of the disease. Apolipoprotein A-I (apoA-I), the major component of high density lipoprotein, is involved in reverse cholesterol transport of lipid metabolism. Recently, it has been found that apoA-I suppresses inflammation via repression of inflammatory cytokine expression; the mechanisms of the apoA-I-suppressive action, however, are not yet well characterized. In this study, we have for the first time found that apoA-I suppresses the expression of some inflammatory cytokines induced by lipopolysaccharide via a specific post-transcriptional regulation process, namely mRNA destabilization, in macrophages. Our further studies have also shown that AU-rich elements in the 3'-untranslated region of TNF-α mRNA are responsive to the apoA-I-mediated mRNA destabilization. The apoA-I-induced inflammatory cytokine mRNA destabilization was associated with increased expression of mRNA-destabilizing protein tristetraprolin through a JAK2/STAT3 signaling pathway-dependent manner. When blocking interaction of apoA-I with ATP-binding membrane cassette transporter A1 (ABCA1), a major receptor for apoA-I in macrophages, it would almost totally abolish the effect of apoA-I on tristetraprolin expression. These results present not only a novel mechanism for the apoA-I-mediated inflammation suppression in macrophages but also provide new insights for developing strategies for modulating vascular inflammation and atherosclerosis.

Indexed as

Gene Expression Regulation3' Untranslated RegionsAdenosine TriphosphateApolipoprotein A-ICholesterolCytokinesHumansInflammationProtein BindingRNA, MessengerRNA Processing, Post-TranscriptionalSignal TransductionSodium-Potassium-Exchanging ATPaseSTAT3 Transcription FactorTristetraprolin3' Untranslated RegionsAdenosine TriphosphateApolipoprotein A-IATP1A1 protein, humanCholesterolCytokinesRNA, MessengerSodium-Potassium-Exchanging ATPaseSTAT3 protein, humanSTAT3 Transcription FactorTristetraprolin

Identifiers

PMID21339300
PMCPMC3077584
OpenAlexW2087465861

What OpenQuestion holds

Textmetadata
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.