Evidence map›Paper›PMID 34420157›Full record

ArticleInflammation2021

ATN-161 Ameliorates Ischemia/Reperfusion-induced Oxidative Stress, Fibro-inflammation, Mitochondrial damage, and Apoptosis-mediated Tight Junction Disruption in bEnd.3 Cells.

Narayanappa Amruta, Gregory Bix

Open access · bronzeAbstract read
In one paragraph

Article in Inflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 39 citations in OpenAlex.

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  16. Aging · 2024
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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.

Narayanappa AmrutaDepartment of Neurosurgery, Clinical Neuroscience Research Center, Tulane University School of Medicine, Room 1349, 131 S. Robertson, Ste 1300, New Orleans, LA, 70112, USA.
Gregory BixDepartment of Neurosurgery, Clinical Neuroscience Research Center, Tulane University School of Medicine, Room 1349, 131 S. Robertson, Ste 1300, New Orleans, LA, 70112, USA. gbix@tulane.edu.ORCID http://orcid.org/0000-0002-8969-9553
Tulane University · US

Funding

Perlecan Domain V is a Novel Promoter of Brain Repair after StrokeR01NS065842 · NINDS · UNIVERSITY OF KENTUCKY · PI BIX, GREGORY JAYE · 2010 to 2019
$3.2M
NIH HHS NS065842NINDS NIH HHS R01 NS065842
6 · The paper itself

Abstract

We have previously demonstrated the significance of endothelial cell-expressed α5β1 integrin in ischemic stroke, having shown that α5β1 integrin endothelial cell-selective knockout mice are significantly resistance to ischemic stroke injury via preservation of the tight junction protein claudin-5 and subsequent stabilization of the blood-brain barrier (BBB). In addition, inhibition of α5β1 by the small peptide noncompetitive integrin α5 inhibitor, ATN-161, is beneficial in a mouse model of ischemic stroke through reduction of infarct volume, edema, stabilization of the BBB, and reduced inflammation and immune cell infiltration into the brain. In continuation with our previous findings, we have further evaluated the mechanistic role of ATN-161 in vitro and found that oxygen and glucose deprivation and reperfusion (OGD/R)-induced inflammation, oxidative stress, apoptosis, mitochondrial depolarization, and fibrosis attenuate tight junction integrity via induction of α5, NLRP3, p-FAK, and p-AKT signaling in mouse brain endothelial cells. ATN-161 treatment (10 µM) effectively inhibited OGD/R-induced extracellular matrix (ECM) deposition by reducing integrin α5, MMP-9, and fibronectin expression, as well as reducing oxidative stress by reducing mitochondrial superoxide radicals, intracellular ROS, inflammation by reducing NLRP3 inflammasome, tight junction loss by reducing claudin-5 and ZO-1 expression levels, mitochondrial damage by inhibiting mitochondrial depolarization, and apoptosis via regulation of p-FAK and p-AKT levels. Taken together, our results further support therapeutically targeting α5 integrin with ATN-161, a safe, well-tolerated, and clinically validated peptide, in ischemic stroke.

Indexed as

AnimalsAnti-Inflammatory AgentsAntioxidantsApoptosisBrainCell HypoxiaCell LineEndothelial CellsFibrosisGlucoseInflammation MediatorsIschemic StrokeMembrane Potential, MitochondrialMiceMitochondriaNeuroinflammatory Diseasesacetyl-prolyl-histidyl-seryl-cysteinyl-asparaginamideAnti-Inflammatory AgentsAntioxidantsGlucoseInflammation Mediatorsintegrin alphavbeta1OligopeptidesReactive Oxygen SpeciesReceptors, VitronectinATN-161bEND.3 cellsFibrosisMitochondrial integrityNLRP3OGD/R

Identifiers

PMID34420157
PMCPMC8380192
OpenAlexW3194649182

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.