Evidence map›Paper›PMID 28550522›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2017

Reduced monocyte adhesion to aortae of diabetic plasminogen activator inhibitor-1 knockout mice.

Ruozhi Zhao, Khuong Le, Mohammed H Moghadasian, Garry X Shen

Abstract read
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In one paragraph

Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 10 citations in OpenAlex.

  1. Endothelial-specific Enhancer as a Cis Element ofCurrent pharmaceutical design · 2024
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  2. Article
  3. Molecular biomarkers of Graves' ophthalmopathy.Experimental and molecular pathology · 2019
    Review
  4. Review
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 1 institution in 1 country.

Ruozhi ZhaoDiabetes Research Group, Department of Internal Medicine, University of Manitoba, 835-715 McDermot Ave, Winnipeg, MB R3E 3P4, Canada.
Khuong LeHuman Nutritional Science, University of Manitoba, Winnipeg, Canada.
Mohammed H MoghadasianHuman Nutritional Science, University of Manitoba, Winnipeg, Canada.
Garry X ShenDiabetes Research Group, Department of Internal Medicine, University of Manitoba, 835-715 McDermot Ave, Winnipeg, MB R3E 3P4, Canada. garry.shen@umanitoba.ca.ORCID http://orcid.org/0000-0001-6947-6400
University of Manitoba · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

OBJECTIVE AND

designTo determine the requirement of plasminogen activator inhibitor-1-knockout (PAI-1) for monocyte adhesion in animals and cells under diabetic conditions. METHODS AND SUBJECTS: Monocyte adhesion assay, enzyme-linked immunosorbent assay, and Western blotting were used in analyzing samples from PAI-1-knockout (PAI-1-KO) mice or cultured human umbilical vein endothelial cells (HUVEC). TREATMENTS: Diabetes in PAI-1-KO and wild-type mice was induced by intraperitoneal injection of streptozotocin (STZ). HUVEC was transfected with short interference RNA (siRNA) against PAI-1, tumor necrosis factor-α (TNFα), or toll-like receptor (TLR4), and then was treated with glycated low-density lipoproteins (glyLDL).

resultsThe adhesion of monocytes to aortic intima was reduced in PAI-1-KO mice, which was associated with decreased levels of TNFα and monocyte chemotactic protein-1 (MCP-1) in plasma and cardiovascular tissue, and increased abundances of urokinase plasminogen activator (uPA) and uPA receptor (uPAR) in cardiovascular tissue compared to wild-type mice. Significant reductions in monocyte adhesion, inflammatory, and fibrinolytic regulators were detected in cardiovascular tissue or plasma in diabetic PAI-1-KO mice compared to wild-type diabetic mice. Transfection of PAI-1, TNFα or TLR4 siRNA to HUVEC inhibited glyLDL-induced monocyte adhesion to EC. PAI-1 siRNA inhibited the abundances of TLR4 and TNFα in EC.

conclusionThe findings suggest that PAI-1 is required for diabetes-induced monocyte adhesion via interactions with uPA/uPAR, and it also regulates TLR4 and TNFα expression in vascular EC. Inhibition of PAI-1 potentially reduces vascular inflammation under diabetic condition.

Indexed as

AnimalsAntigensAortaCell AdhesionChemokine CCL2Diabetes Mellitus, ExperimentalHumansHuman Umbilical Vein Endothelial CellsMaleMice, Inbred C57BLMice, KnockoutMonocytesReceptors, Urokinase Plasminogen ActivatorRNA, Small InterferingSerpin E2Toll-Like Receptor 4AntigensCcl2 protein, mouseChemokine CCL2Receptors, Urokinase Plasminogen ActivatorRNA, Small InterferingSerpin E2Serpine2 protein, mouseTLR4 protein, humanToll-Like Receptor 4Tumor Necrosis Factor-alphaUrokinase-Type Plasminogen ActivatorMonocyte adhesionPlasminogen activator inhibitor-1 knockout miceStreptozotocin-induced diabetesToll-like receptor-4Tumor necrosis factor-α

Identifiers

PMID28550522
OpenAlexW2620178746

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.