Evidence map›Paper›PMID 24965120›Full record

ArticleBMC neuroscience2014

HIV-1 Tat C phosphorylates VE-cadherin complex and increases human brain microvascular endothelial cell permeability.

Ritu Mishra, Sunit Kumar Singh

Open access · goldAbstract read
In one paragraph

Article in BMC neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
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  9. Article
  10. Functional impact of HIV-1 Tat on cells of the CNS and its role in HAND.Cellular and molecular life sciences : CMLS · 2020
    Review
  11. Opioid and neuroHIV Comorbidity - Current and Future Perspectives.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2020
    Review
  12. Polydatin protects against lipopolysaccharide-induced endothelial barrier disruption via SIRT3 activation.Laboratory investigation; a journal of technical methods and pathology · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Endothelial cell-cell adhesion and signaling.Experimental cell research · 2017
    Review
  17. Article
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  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Ritu Mishra
Sunit Kumar SinghLaboratory of Neurovirology and Inflammation Biology, CSIR-Centre for Cellular and Molecular Biology (CCMB), Uppal Road, Hyderabad 500007, India. sunitsingh2000@gmail.com.
Centre for Cellular and Molecular Biology · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundHuman brain microvascular endothelial cells (hBMVECs) are integral part of the blood brain barrier. Post-translational modifications of adherens junction proteins regulate the permeability of human brain microvascular endothelial cells. Pro-inflammatory signals can induce tyrosine phosphorylation of adherens junction proteins. The primary objective of this work is to provide a molecular model; how the HIV-1 Tat protein can compromise the BBB integrity and eventually lead to neurological consequences. We exposed hBMVECs to recombinant HIV-1 clade C Tat protein to study the effect of HIV-1 Tat C on permeability of hBMVECs. Trans-endothelial electrical resistance and fluorescent dye migration assay have been used to check the permeability of hBMVECs. DCFDA staining has been used for intracellular reactive oxygen species (ROS) detection. Western blotting has been used to study the expression levels and co-immunoprecipitation has been used to study the interactions among adherens junction proteins.

resultsHIV-1 Tat C protein induced NOX2 and NOX4 expression level and increased intracellular ROS level. Redox-sensitive kinase; PYK2 activation led to increased tyrosine phosphorylation of VE-cadherin and β-catenin, leading to disruption of junctional assembly. The dissociation of tyrosine phosphatases VE-PTP and SHP2 from cadherin complex resulted into increased tyrosine phosphorylation of VE-cadherin and β-catenin in HIV-1 Tat C treated hBMVECs.

conclusionUnrestricted phosphorylation of junctional proteins in hBMVECs, in response to HIV-1 Tat C protein; leads to the disruption of junctional complexes and increased endothelial permeability.

Indexed as

Antigens, CDbeta CateninBlood-Brain BarrierBlotting, WesternBrainCadherin 5CadherinsCapillary PermeabilityCells, CulturedElectric ImpedanceEndothelial CellsEndothelium, VascularFluoresceinsFluorescent DyesHIV-1HumansAntigens, CDbeta CateninCadherin 5CadherinsCTNNB1 protein, humandiacetyldichlorofluoresceinFluoresceinsFluorescent DyesReactive Oxygen Speciestat Gene Products, Human Immunodeficiency Virus

Identifiers

PMID24965120
PMCPMC4230799
OpenAlexW2038016863

What OpenQuestion holds

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LicenceCC BY
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.