Evidence map›Paper›PMID 26473731›Full record

ArticlePloS one2015

Synthetic Oligodeoxynucleotides Containing Multiple Telemeric TTAGGG Motifs Suppress Inflammasome Activity in Macrophages Subjected to Oxygen and Glucose Deprivation and Reduce Ischemic Brain Injury in Stroke-Prone Spontaneously Hypertensive Rats.

Jing Zhao, Yongshan Mou, Joshua D Bernstock, Dace Klimanis, Sixian Wang, Maria Spatz, Dragan Maric, Kory Johnson, Dennis M Klinman, Xiaohong Li and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. An integrated investigation of systemic and localized pathophysiological mechanisms of stroke and multimodal therapeutic strategies.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2026
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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

12 authors at 5 institutions in 2 countries.

Jing ZhaoDepartment of Neurology, Jinan Central Hospital affiliated with Shandong University, 105 Jiefang Road, Jinan, Shandong, 250013, P. R. China; Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America.
Yongshan MouStroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America.
Joshua D BernstockStroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America.
Dace KlimanisStroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America.
Sixian WangCollege of Arts and Sciences, Cornell University, Ithaca, New York, United States of America.
Maria SpatzStroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America.
Dragan MaricNational Institute of Neurological Disorders and Stroke, Flow Cytometry Core Facility, Bethesda, Maryland, United States of America.
Kory JohnsonInformation Technology & Bioinformatics Program, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America.
Dennis M KlinmanCancer and Inflammation Program, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Xiaohong LiDepartment of Neurology, Jinan Central Hospital affiliated with Shandong University, 105 Jiefang Road, Jinan, Shandong, 250013, P. R. China.
Xinhui LiStroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America.
John M HallenbeckStroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America.
National Institute of Neurological Disorders and Stroke · USNational Institutes of Health · USFlorida State University · USNational Cancer Institute · USShandong University · CN

Funding

Protective Mechanisms In Cerebral IschemiaZIANS002924 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI HALLENBECK, JOHN · 2009 to 2018
$16.5M
Hibernation--a New Approach To Stroke TherapyZIANS002856 · NINDS · NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE · PI HALLENBECK, JOHN · 2009 to 2018
$9.9M
Mechanism of action and therapeutic utility of immunosuppressive oligonucleotideZIABC010853 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KLINMAN, DENNIS · 2009 to 2019
$3.8M
Intramural NIH HHS
6 · The paper itself

Abstract

The immune system plays a fundamental role in both the development and pathobiology of stroke. Inflammasomes are multiprotein complexes that have come to be recognized as critical players in the inflammation that ultimately contributes to stroke severity. Inflammasomes recognize microbial and host-derived danger signals and activate caspase-1, which in turn controls the production of the pro-inflammatory cytokine IL-1β. We have shown that A151, a synthetic oligodeoxynucleotide containing multiple telemeric TTAGGG motifs, reduces IL-1β production by activated bone marrow derived macrophages that have been subjected to oxygen-glucose deprivation and LPS stimulation. Further, we demonstrate that A151 reduces the maturation of caspase-1 and IL-1β, the levels of both the iNOS and NLRP3 proteins, and the depolarization of mitochondrial membrane potential within such cells. In addition, we have demonstrated that A151 reduces ischemic brain damage and NLRP3 mRNA levels in SHR-SP rats that have undergone permanent middle cerebral artery occlusion. These findings clearly suggest that the modulation of inflammasome activity via A151 may contribute to a reduction in pro-inflammatory cytokine production by macrophages subjected to conditions that model brain ischemia and modulate ischemic brain damage in an animal model of stroke. Therefore, modulation of ischemic pathobiology by A151 may have a role in the development of novel stroke prevention and therapeutic strategies.

Indexed as

Nucleotide MotifsTelomereAnimalsBrain IschemiaCarrier ProteinsCaspase 1GlucoseInflammasomesInterleukin-1betaMacrophagesNLR Family, Pyrin Domain-Containing 3 ProteinOligodeoxyribonucleotidesOxygenRatsRats, Inbred SHRCarrier ProteinsCaspase 1CPG-oligonucleotideGlucoseIL1B protein, ratInflammasomesInterleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratOligodeoxyribonucleotidesOxygen

Identifiers

PMID26473731
PMCPMC4608557
OpenAlexW2338396143

What OpenQuestion holds

Textmetadata
LicenceCC0
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.