Evidence map›Paper›PMID 19674747›Full record

ArticleAtherosclerosis2010

Non-nucleoside reverse transcriptase inhibitor efavirenz increases monolayer permeability of human coronary artery endothelial cells.

Md Saha Jamaluddin, Peter H Lin, Qizhi Yao, Changyi Chen

Abstract read
In one paragraph

Article in Atherosclerosis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.1field-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

21 citing papers in PubMed, 40 citations in OpenAlex.

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  19. Brief report: Endothelial colony-forming cells and inflammatory monocytes in HIV.Journal of acquired immune deficiency syndromes (1999) · 2015
    Article
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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 2 institutions in 1 country.

Md Saha JamaluddinMolecular Surgeon Research Center, Division of Vascular Surgery and Endovascular Therapy, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
Peter H Lin
Qizhi Yao
Changyi Chen
Baylor College of Medicine · USMichael E. DeBakey VA Medical Center · US

Funding

HIV PROTEASE INHIBITORS EFFECT--NENDOTHELIAL DYSFUNCTIONR01HL065916 · NHLBI · EMORY UNIVERSITY · PI CHEN, CHANGYI · 2000 to 2004
$1.8M
Effects of HIV Protease Inhibitors of Endothelial BarrieR01HL072716 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI CHEN, CHANGYI · 2002 to 2005
$1.2M
Influenza HA in SHIV VLPS for mucosal vaccinationR01DE015543 · NIDCR · BAYLOR COLLEGE OF MEDICINE · PI YAO, QIZHI C. · 2003 to 2006
$1.2M
NHLBI NIH HHS HL65916NHLBI NIH HHS HL72716NHLBI NIH HHS R01 HL065916NHLBI NIH HHS R01 HL072716NIDCR NIH HHS DE15543NIDCR NIH HHS R01 DE015543
6 · The paper itself

Abstract

Highly active antiretroviral therapy (HAART) is often associated with endothelial dysfunction and cardiovascular complications. In this study, we determined whether HIV non-nucleoside reverse transcriptase inhibitor efavirenz (EFV) could increase endothelial permeability. Human coronary artery endothelial cells (HCAECs) were treated with EFV (1, 5 and 10 microg/ml) and endothelial permeability was determined by a transwell system with a fluorescence-labeled dextran tracer. HCAECs treated with EFV showed a significant increase of endothelial permeability in a concentration-dependent manner. With real time PCR analysis, EFV significantly reduced the mRNA levels of tight junction proteins claudin-1, occludin, zonula occluden-1 and junctional adhesion molecule-1 compared with controls (P<0.05). Protein levels of these tight junction molecules were also reduced substantially in the EFV-treated cells by western blot and flow cytometry analyses. In addition, EFV also increased superoxide anion production with dihydroethidium and cellular glutathione assays, while it decreased mitochondrial membrane potential with JC-staining. Antioxidants (ginkgolide B and MnTBAP) effectively blocked EFV-induced endothelial permeability and mitochondrial dysfunction. Furthermore, EFV increased the phosphorylation of MAPK JNK and IkappaBalpha, thereby increasing NFkappaB translocation to the nucleus. Chemical JNK inhibitor and dominant negative mutant JNK and IkappaBalpha adenoviruses effectively blocked the effects of EFV on HCAECs. Thus, EFV increases endothelial permeability which may be due to the decrease of tight junction proteins and the increase of superoxide anion. JNK and NFkappaB activation may be directly involved in the signal transduction pathway of EFV action in HCAECs.

Indexed as

AlkynesBenzoxazinesCapillary PermeabilityCells, CulturedCoronary VesselsCyclopropanesEndothelium, VascularHumansReverse Transcriptase InhibitorsAlkynesBenzoxazinesCyclopropanesefavirenzReverse Transcriptase Inhibitors

Identifiers

PMID19674747
PMCPMC2813420
OpenAlexW2071354625

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.