Evidence map›Paper›PMID 19766117›Full record

ArticleExperimental neurology2009

Overexpression of human selenoprotein H in neuronal cells ameliorates ultraviolet irradiation-induced damage by modulating cell signaling pathways.

Natalia Mendelev, Sam Witherspoon, P Andy Li

Abstract read
In one paragraph

Article in Experimental neurology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
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  8. Selenoprotein H is an essential regulator of redox homeostasis that cooperates with p53 in development and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  9. Article
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  17. Selenium. Role of the essential metalloid in health.Metal ions in life sciences · 2013
    Review
  18. Article
  19. Article
  20. Regulation of redox signaling by selenoproteins.Biological trace element research · 2010
    Article
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

3 authors at 1 institution in 1 country.

Natalia MendelevDepartment of Pharmaceutical Sciences, Biomanufacturing Research Institute and Technological Enterprise (BRITE), North Carolina Central University, 302 East Lawson Street, Durham, NC 27707, USA.
Sam Witherspoon
P Andy Li
North Carolina Central University · US

Funding

Role of UCP2 in Diabetic Stroke BrainR01DK075476 · NIDDK · NORTH CAROLINA CENTRAL UNIVERSITY · PI LI, P. ANDY · 2007 to 2011
$1.2M
NIDDK NIH HHS R01 DK075476NIDDK NIH HHS R01DK075476
6 · The paper itself

Abstract

Selenoprotein H (SelH) is one of the 25 so far identified selenoproteins. Selenoproteins may function as antioxidants, heavy metal antidotes, and neural survival factors. Previous studies have shown that overexpression of SelH in HT22 cells protected the cells from UVB irradiation-induced death by reducing superoxide formation. The objective of this study was to determine the effects of SelH on cell signaling pathways after UVB irradiation. We exposed both human SelH- and vector-transfected HT22 cells to UVB irradiation and collected samples at 5 and 17 h of recovery. Cell viability was assessed, as well as protein levels of caspase-3, -8, -9, apoptosis-inducing factor (AIF), P53, nuclear respiratory factor-1 (NRF-1) and heat shock protein 40 (HSP40). Mitochondrial membrane potential was determined by flow cytometry. Overexpression of SelH protected cells against UVB-induced injury by blockade of the mitochondria-initiated cell death pathway, prevention of mitochondrial membrane depolarization, and suppression of the increase of p53. Furthermore, overexpression of SelH increased levels of NRF-1, an antioxidant, and HSP40, a protein chaperone that repairs denatured protein. We conclude that SelH protects neurons against UVB-induced damage by inhibiting apoptotic cell death pathways, by preventing mitochondrial depolarization, and by promoting cell survival pathways.

Indexed as

Ultraviolet RaysAnimalsApoptosisBlotting, WesternCaspase 3Caspase 9Cell LineCell SurvivalDNA-Binding ProteinsGene ExpressionGenetic VectorsHSP40 Heat-Shock ProteinsHumansMembrane PotentialsMiceMitochondrial MembranesCaspase 3Caspase 9DNA-Binding ProteinsHSP40 Heat-Shock ProteinsNuclear Respiratory Factor 1selenoprotein H, humanSelenoproteinsTumor Suppressor Protein p53

Identifiers

PMID19766117
PMCPMC2784002
OpenAlexW2047562699

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.