Evidence map›Paper›PMID 27167771›Full record

ArticleEndocrinology2016

Effects of Oxidative Stress and Testosterone on Pro-Inflammatory Signaling in a Female Rat Dopaminergic Neuronal Cell Line.

Shaletha Holmes, Meharvan Singh, Chang Su, Rebecca L Cunningham

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

37 citing papers in PubMed, 66 citations in OpenAlex.

  1. Review
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  7. Chronic intermittent hypoxia-induced hypertension: the impact of sex hormones.American journal of physiology. Regulatory, integrative and comparative physiology · 2024
    Review
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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

4 authors at 2 institutions in 1 country.

Shaletha HolmesDepartment of Pharmacology and Neuroscience, Institute for Aging and Alzheimer's Disease Research, University of North Texas Health Science Center, Fort Worth, Texas 76107.
Meharvan SinghDepartment of Pharmacology and Neuroscience, Institute for Aging and Alzheimer's Disease Research, University of North Texas Health Science Center, Fort Worth, Texas 76107.
Chang SuDepartment of Pharmacology and Neuroscience, Institute for Aging and Alzheimer's Disease Research, University of North Texas Health Science Center, Fort Worth, Texas 76107.
Rebecca L CunninghamDepartment of Pharmacology and Neuroscience, Institute for Aging and Alzheimer's Disease Research, University of North Texas Health Science Center, Fort Worth, Texas 76107.
University of North Texas · USUniversity of North Texas Health Science Center · US

Funding

ROLE OF MITHOCHONDRIAL ERB IN NEURONAL VULNDERABILITY TO NEUROTOXIC STRESSP01AG027956 · NIA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI SINGH, MEHARVAN · 2007 to 2017
$11.3M
Training in the Neurobiology of Aging and Alzheimer's DiseaseT32AG020494 · NIA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI ROBERT Clinton BARBER, NATHALIE SUMIEN · 2002 to 2026
$6.9M
Interactions between testosterone and oxidative stress in dopamine neuronsR01NS091359 · NINDS · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI CUNNINGHAM, REBECCA L · 2015 to 2019
$1.6M
NIA NIH HHS P01 AG027956NIA NIH HHS T32 AG020494NINDS NIH HHS R01 NS091359
6 · The paper itself

Abstract

Parkinson's disease, a progressive neurodegenerative disorder, is associated with oxidative stress and neuroinflammation. These pathological markers can contribute to the loss of dopamine neurons in the midbrain. Interestingly, men have a 2-fold increased incidence for Parkinson's disease than women. Although the mechanisms underlying this sex difference remain elusive, we propose that the primary male sex hormone, testosterone, is involved. Our previous studies show that testosterone, through a putative membrane androgen receptor, can increase oxidative stress-induced neurotoxicity in dopamine neurons. Based on these results, this study examines the role of nuclear factor κ B (NF-κB), cyclooxygenase-2 (COX2), and apoptosis in the deleterious effects of androgens in an oxidative stress environment. We hypothesize, under oxidative stress environment, testosterone via a putative membrane androgen receptor will exacerbate oxidative stress-induced NF-κB/COX2 signaling in N27 dopaminergic neurons, leading to apoptosis. Our data show that testosterone increased the expression of COX2 and apoptosis in dopamine neurons. Inhibiting the NF-κB and COX2 pathway with CAPE and ibuprofen, respectively, blocked testosterone's negative effects on cell viability, indicating that NF-κB/COX2 cascade plays a role in the negative interaction between testosterone and oxidative stress on neuroinflammation. These data further support the role of testosterone mediating the loss of dopamine neurons under oxidative stress conditions, which may be a key mechanism contributing to the increased incidence of Parkinson's disease in men compared with women.

Indexed as

AnimalsApoptosisCaffeic AcidsCell LineCyclooxygenase 2Cyclooxygenase InhibitorsDopaminergic NeuronsFemaleIbuprofenInflammationNF-kappa BOxidative StressPhenylethyl AlcoholRatsSignal TransductionTestosteronecaffeic acid phenethyl esterCaffeic AcidsCyclooxygenase 2Cyclooxygenase InhibitorsIbuprofenNF-kappa BPhenylethyl AlcoholTestosterone

Identifiers

PMID27167771
PMCPMC4929547
OpenAlexW2388718727

What OpenQuestion 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 OpenQuestion graph.