Evidence map›Paper›PMID 21659524›Full record

ArticleThe Journal of biological chemistry2011

High glucose-treated macrophages augment E-selectin expression in endothelial cells.

Te-Chuan Chen, Shao-Ju Chien, Hsing-Chun Kuo, Wen-Shih Huang, Jiunn-Ming Sheen, Tseng-Hsi Lin, Chia-Kuang Yen, Mao-Lin Sung, Cheng-Nan Chen

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. 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

9 authors at 6 institutions in 1 country.

Te-Chuan ChenDivision of Nephrology, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Shao-Ju Chien
Hsing-Chun Kuo
Wen-Shih Huang
Jiunn-Ming Sheen
Tseng-Hsi Lin
Chia-Kuang Yen
Mao-Lin Sung
Cheng-Nan Chen
St. Martin de Porres Hospital · TWChang Gung Memorial Hospital · TWChang Gung University · TWChiayi Chang Gung Memorial Hospital · TWNational Chiayi University · TWTaichung Veterans General Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

E-selectin expression by endothelial cells (ECs) is crucial for leukocyte recruitment during the inflammatory response. Macrophage accumulation and serum E-selectin elevation are features of type 2 diabetes mellitus. However, the interactions between macrophages and ECs in regulating vascular endothelial function are not clearly understood. We investigated the mechanisms underlying the modulation of EC E-selectin expression by high glucose (HG)-treated macrophages. Macrophage-conditioned media (MCM) were prepared from HG-treated macrophages. EC stimulation with HG-MCM induced increases the expression and secretion of E-selectin. By using specific inhibitors and small interfering RNAs, we demonstrate that the activation of the JNK and p38 MAPK pathways are critical for HG-MCM-induced E-selectin expression. Transcription factor ELISA and chromatin immunoprecipitation assays further showed that HG-MCM increases the NF-κB- and AP-1 DNA-binding activities in ECs. The inhibition of NF-κB and AP-1 activation by specific siRNAs blocks the HG-MCM-induced E-selectin promoter activity and expression. Protein arrays and blocking assays using neutralizing antibodies demonstrated that macrophage inflammatory protein 1α and 1β in HG-MCM are major mediators for the induction of EC E-selectin expression. These data support the hypothesis that E-selectin up-regulation stimulated by macrophages may play an active role in atherogenesis in the HG condition and suggest a new mechanism by which arterial disease is accelerated in diabetes.

Indexed as

Antibodies, NeutralizingBinding SitesCell AdhesionCell LineChemokine CCL3Chemokine CCL4Culture Media, ConditionedDose-Response Relationship, DrugEndothelial CellsE-SelectinGene Expression RegulationGlucoseHumansJNK Mitogen-Activated Protein KinasesMacrophagesMAP Kinase Signaling SystemAntibodies, NeutralizingCCL3 protein, humanChemokine CCL3Chemokine CCL4Culture Media, ConditionedE-SelectinGlucoseJNK Mitogen-Activated Protein KinasesNF-kappa Bp38 Mitogen-Activated Protein KinasesTranscription Factor AP-1

Identifiers

PMID21659524
PMCPMC3138282
OpenAlexW2027915075

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.