Evidence map›Paper›PMID 21816823›Full record

ArticleThe Journal of biological chemistry2011

Deregulation of microRNAs by HIV-1 Vpr protein leads to the development of neurocognitive disorders.

Ruma Mukerjee, J Robert Chang, Luis Del Valle, Asen Bagashev, Monika M Gayed, Randolph B Lyde, Brian J Hawkins, Eugen Brailoiu, Eric Cohen, Chris Power and 3 more

Erratum issuedOpen 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. An erratum has been issued. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.5field-weighted citation impact, top 21% 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

35 citing papers in PubMed, 53 citations in OpenAlex.

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  15. miR-34a in Neurophysiology and Neuropathology.Journal of molecular neuroscience : MN · 2019
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 6 institutions in 2 countries.

Ruma MukerjeeDepartment of Neurology, Molecular Studies of Neurodegenerative Diseases Laboratory, Temple University School of Medicine, Philadelphia, Pennsylvania 19140, USA.
J Robert Chang
Luis Del Valle
Asen Bagashev
Monika M Gayed
Randolph B Lyde
Brian J Hawkins
Eugen Brailoiu
Eric Cohen
Chris Power
S Ausim Azizi
Benjamin B Gelman
Bassel E Sawaya
Temple University · USLouisiana State University · USThe University of Texas Medical Branch at Galveston · USUniversité de Montréal · CAUniversity of Alberta · CAUniversity of Washington · US

Funding

HARVARD CLINICAL AND TRANSLATIONAL SCIENCE CENTER (UL1)UL1RR025758 · NCRR · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2008 to 2011
$91.4M
National NeuroAIDS Tissue Consortium Statistics and Data Coordinating CenterU01MH083545 · NIMH · INDIANA UNIVERSITY INDIANAPOLIS · PI YIANNOUTSOS, CONSTANTIN THEODORE · 2008 to 2012
$3.3M
Role of p53 family in neuropathogenesis in AIDSR01NS059327 · NINDS · TEMPLE UNIV OF THE COMMONWEALTH · PI SAWAYA, BASSEL E · 2008 to 2012
$1.9M
Regulation of vascular inflammation by mitochondrial reactive oxygen speciesR00HL094536 · NHLBI · UNIVERSITY OF WASHINGTON · PI HAWKINS, BRIAN J. · 2010 to 2012
$744k
NCRR NIH HHS UL1 RR 025758NCRR NIH HHS UL1 RR025758NHLBI NIH HHS R00 HL094536NIMH NIH HHS U01 MH083545NINDS NIH HHS R01 NS059327NINDS NIH HHS R01-NS059327
6 · The paper itself

Abstract

Studies have shown that HIV-infected patients develop neurocognitive disorders characterized by neuronal dysfunction. The lack of productive infection of neurons by HIV suggests that viral and cellular proteins, with neurotoxic activities, released from HIV-1-infected target cells can cause this neuronal deregulation. The viral protein R (Vpr), a protein encoded by HIV-1, has been shown to alter the expression of various important cytokines and inflammatory proteins in infected and uninfected cells; however the mechanisms involved remain unclear. Using a human neuronal cell line, we found that Vpr can be taken up by neurons causing: (i) deregulation of calcium homeostasis, (ii) endoplasmic reticulum-calcium release, (iii) activation of the oxidative stress pathway, (iv) mitochondrial dysfunction and v- synaptic retraction. In search for the cellular factors involved, we performed microRNAs and gene array assays using human neurons (primary cultures or cell line, SH-SY5Y) that we treated with recombinant Vpr proteins. Interestingly, Vpr deregulates the levels of several microRNAs (e.g. miR-34a) and their target genes (e.g. CREB), which could lead to neuronal dysfunctions. Therefore, we conclude that Vpr plays a major role in neuronal dysfunction through deregulating microRNAs and their target genes, a phenomenon that could lead to the development of neurocognitive disorders.

Indexed as

Gene Expression Regulation, ViralAnimalsCalciumCognition DisordersHumansImmunohistochemistryMiceMice, TransgenicMicroRNAsMicroscopy, FluorescenceMitochondriaNervous System DiseasesNeuronsOxidative Stressvpr Gene Products, Human Immunodeficiency VirusCalciumMicroRNAsvpr Gene Products, Human Immunodeficiency Virus

Identifiers

PMID21816823
PMCPMC3186354
OpenAlexW2001581901

What Socratic 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 Socratic graph.