Evidence map›Paper›PMID 26469385›Full record

ArticleScientific reports2015

The HIV matrix protein p17 induces hepatic lipid accumulation via modulation of nuclear receptor transcriptoma.

Barbara Renga, Daniela Francisci, Adriana Carino, Silvia Marchianò, Sabrina Cipriani, Maria Chiara Monti, Rachele Del Sordo, Elisabetta Schiaroli, Eleonora Distrutti, Franco Baldelli and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.3field-weighted citation impact, top 39% 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

3 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Review
  3. 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

11 authors at 3 institutions in 1 country.

Barbara RengaDepartment of Surgical and Biomedical Sciences, Section of gastroenterology, University of Perugia, Perugia, Italy.
Daniela FrancisciDepartment of Medicine, Section of Infectious diseases, University of Perugia, Perugia, Italy.
Adriana CarinoDepartment of Surgical and Biomedical Sciences, Section of gastroenterology, University of Perugia, Perugia, Italy.
Silvia MarchianòDepartment of Surgical and Biomedical Sciences, Section of gastroenterology, University of Perugia, Perugia, Italy.
Sabrina CiprianiDepartment of Medicine, Section of Infectious diseases, University of Perugia, Perugia, Italy.
Maria Chiara MontiDepartment of Biomedical and Pharmaceutical Sciences, University of Salerno, Fisciano, Italy.
Rachele Del SordoDepartment of Experimental Medicine and Biochemical Sciences, Section of Anatomic Pathology and Histology, University of Perugia, Perugia, Italy.
Elisabetta SchiaroliDepartment of Medicine, Section of Infectious diseases, University of Perugia, Perugia, Italy.
Eleonora DistruttiHospital S.M. Misericordia, Perugia, Italy.
Franco BaldelliDepartment of Medicine, Section of Infectious diseases, University of Perugia, Perugia, Italy.
Stefano FiorucciDepartment of Surgical and Biomedical Sciences, Section of gastroenterology, University of Perugia, Perugia, Italy.
University of Perugia · ITAzienda Ospedaliera di Perugia · ITUniversity of Salerno · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Liver disease is the second most common cause of mortality in HIV-infected persons. Exactly how HIV infection per se affects liver disease progression is unknown. Here we have investigated mRNA expression of 49 nuclear hormone receptors (NRs) and 35 transcriptional coregulators in HepG2 cells upon stimulation with the HIV matrix protein p17. This viral protein regulated mRNA expression of some NRs among which LXRα and its transcriptional co-activator MED1 were highly induced at mRNA level. Dissection of p17 downstream intracellular pathway demonstrated that p17 mediated activation of Jak/STAT signaling is responsible for the promoter dependent activation of LXR. The treatment of both HepG2 as well as primary hepatocytes with HIV p17 results in the transcriptional activation of LXR target genes (SREBP1c and FAS) and lipid accumulation. These effects are lost in HepG2 cells pre-incubated with a serum from HIV positive person who underwent a vaccination with a p17 peptide as well as in HepG2 cells pre-incubated with the natural LXR antagonist gymnestrogenin. These results suggest that HIV p17 affects NRs and their related signal transduction thus contributing to the progression of liver disease in HIV infected patients.

Indexed as

Lipid MetabolismAIDS VaccinesAnimalsCells, CulturedCholesterolenv Gene Products, Human Immunodeficiency VirusHepatocytesHep G2 CellsHIVHumansLiverLiver X ReceptorsMediator Complex Subunit 1MiceMice, Inbred C57BLOrphan Nuclear ReceptorsAIDS VaccinesCholesterolenv Gene Products, Human Immunodeficiency VirusLiver X ReceptorsMED1 protein, humanMediator Complex Subunit 1NR1H3 protein, humanNr1h3 protein, mouseOrphan Nuclear Receptorsp17 gag peptide, human immunodeficiency virusPeptide FragmentsReceptors, Cytoplasmic and NuclearRecombinant ProteinsSTAT Transcription FactorsSterol Regulatory Element Binding Protein 1Trans-Activators

Identifiers

PMID26469385
PMCPMC4606811
OpenAlexW2408985768

What OpenQuestion holds

Textmetadata
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.