Evidence map›Paper›PMID 30139948›Full record

ArticleScientific reports2018

In Vitro Modulation of Redox and Metabolism Interplay at the Brain Vascular Endothelium: Genomic and Proteomic Profiles of Sulforaphane Activity.

Ravi K Sajja, Mohammad A Kaisar, Vikrant Vijay, Varsha G Desai, Shikha Prasad, Luca Cucullo

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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  13. Cerebrovascular and Neurological Disorders: Protective Role of NRF2.International journal of molecular sciences · 2019
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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

6 authors at 3 institutions in 1 country.

Ravi K SajjaDepartment of Pharmaceutical Sciences, Texas Tech University Health Sciences Center, Amarillo, TX, 79106, USA.
Mohammad A KaisarDepartment of Pharmaceutical Sciences, Texas Tech University Health Sciences Center, Amarillo, TX, 79106, USA.
Vikrant VijayDivision of Systems Biology, National Center for Toxicological Research, US FDA, Jefferson, AR, 72079, USA.
Varsha G DesaiDivision of Systems Biology, National Center for Toxicological Research, US FDA, Jefferson, AR, 72079, USA.
Shikha PrasadDepartment of Neurology, Northwestern University - The Feinberg School of Medicine, Chicago, IL, 60611, USA.
Luca CuculloDepartment of Pharmaceutical Sciences, Texas Tech University Health Sciences Center, Amarillo, TX, 79106, USA. luca.cucullo@ttuhsc.edu.ORCID 0000-0002-2827-7162
Texas Tech University · USNational Center for Toxicological Research · USNorthwestern University · US

Funding

Testing tobacco smoke toxicity at the blood-brain barrierR01DA029121 · NIDA · TEXAS TECH UNIVERSITY HEALTH SCIS CENTER · PI ABBRUSCATO, THOMAS J, CUCULLO, LUCA · 2011 to 2021
$3.6M
NIDA NIH HHS R01 DA029121U.S. Department of Health & Human Services | NIH | National Institute on Drug Abuse (NIDA) R01DA029121
6 · The paper itself

Abstract

Sulforaphane (SFN) has been shown to protect the brain vascular system and effectively reduce ischemic injuries and cognitive deficits. Given the robust cerebrovascular protection afforded by SFN, the objective of this study was to profile these effects in vitro using primary mouse brain microvascular endothelial cells and focusing on cellular redox, metabolism and detoxification functions. We used a mouse MitoChip array developed and validated at the FDA National Center for Toxicological Research (NCTR) to profile a host of genes encoded by nuclear and mt-DNA following SFN treatment (0-5 µM). Corresponding protein expression levels were assessed (ad hoc) by qRT-PCR, immunoblots and immunocytochemistry (ICC). Gene ontology clustering revealed that SFN treatment (24 h) significantly up-regulated ~50 key genes (>1.5 fold, adjusted p < 0.0001) and repressed 20 genes (<0.7 fold, adjusted p < 0.0001) belonging to oxidative stress, phase 1 & 2 drug metabolism enzymes (glutathione system), iron transporters, glycolysis, oxidative phosphorylation (OXPHOS), amino acid metabolism, lipid metabolism and mitochondrial biogenesis. Our results show that SFN stimulated the production of ATP by promoting the expression and activity of glucose transporter-1, and glycolysis. In addition, SFN upregulated anti-oxidative stress responses, redox signaling and phase 2 drug metabolism/detoxification functions, thus elucidating further the previously observed neurovascular protective effects of this compound.

Indexed as

Adenosine TriphosphateAnimalsAntioxidantsBlotting, WesternBrainCells, CulturedCell SurvivalEndothelium, VascularFluorescent Antibody TechniqueGenomicsImmunohistochemistryIsothiocyanatesMiceOxidation-ReductionOxidative StressProteomicsAdenosine TriphosphateAntioxidantsIsothiocyanatesReactive Oxygen SpeciessulforaphaneSulfoxides

Identifiers

PMID30139948
PMCPMC6107504
OpenAlexW2887655473

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.