Evidence map›Paper›PMID 20547234›Full record

ArticleNitric oxide : biology and chemistry2010

Differential roles of nitric oxide synthases in regulation of ultraviolet B light-induced apoptosis.

Wei Liu, Shiyong Wu

Open access · greenAbstract read
In one paragraph

Article in Nitric oxide : biology and chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 35 citations in OpenAlex.

  1. Review
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  3. Role of constitutive nitric oxide synthases in the dynamic regulation of the autophagy response of keratinocytes upon UVB exposure.Photochemical & photobiological sciences : Official journal of the European Photochemistry Association and the European Society for Photobiology · 2020
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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

2 authors at 1 institution in 1 country.

Wei LiuDepartment of Chemistry and Biochemistry, Edison Biotechnology Institute and Molecular and Cellular Biology Program, Ohio University, Athens, OH 45701, USA.
Shiyong Wu
Ohio University · US

Funding

UV INDUCED AND PERK MEDIATED SIGNALING PATHWAYSR01CA086928 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI WU, SHIYONG · 2000 to 2012
$2.1M
UV-induced and NOS-mediated Zn elevation, translation regulatin and apoptosis.R56CA086928 · NCI · OHIO UNIVERSITY ATHENS · PI WU, SHIYONG · 2007 to 2007
$206k
NCI NIH HHS 2R01CA086928NCI NIH HHS 2R56CA086928NCI NIH HHS R01 CA086928NCI NIH HHS R56 CA086928
6 · The paper itself

Abstract

Ultraviolet B light (UVB) activates nitric oxide synthase(s) (NOSs) and nitric oxide (NO()) production, which plays a role in regulation of apoptosis. However, the role of NO() in UVB-induced apoptosis remains controversial. In this study, we analyzed expression and activation of constitutive NOSs (cNOSs) and their roles in UV-induced apoptosis of HaCaT keratinocytes. Our data showed that the expression of neuronal NOS (nNOS) was increased while endothelial NOS (eNOS) was uncoupled in the early phase (0-6 h) post-UVB. The expression of both cNOSs peaked at 12h post-UVB and NO() was transiently elevated with 30 min and then steadily rose from 6 to 18 h post-UVB. The expression of iNOS was detected at 6h post-UVB and then sturdily increased. Inhibition of cNOSs with L-NAME reduced the inducibility of NO(*) in the early and late phases of irradiation. Along with the eNOS uncoupling, an increased level of peroxynitrite (ONOO(-)) was detected in the early phase, but not in the late phase post-UVB. Inhibition of cNOSs reduced the production of ONOO(-) in the early time, but led to an increase of ONOO(-) in the late time after UVB-irradiation. The results indicate that cNOSs regulate NO()/ONOO(-) imbalance after UVB-irradiation. Our data suggested that the activation of cNOSs in the early phase post-UVB leads to NO()/ONOO(-) imbalance and promotes apoptosis via a caspase 3-independent pathway. The elevation of NO() in the late phase of UVB-irradiation is mainly produced by inducible NOS (iNOS). However, cNOSs also contribute to the NO() production and to maintain a higher NO()/ONOO(-) ratio, which reduces caspase 3 activity and protects cells from UVB-induced apoptosis.

Indexed as

ApoptosisUltraviolet RaysCell DifferentiationCells, CulturedHumansKeratinocytesNitric OxideNitric Oxide SynthaseNitric OxideNitric Oxide Synthase

Identifiers

PMID20547234
PMCPMC2928404
OpenAlexW2012784844

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.