Evidence map›Paper›PMID 23583926›Full record

ArticleNeuropharmacology2013

Anti-inflammatory effects of angiotensin-(1-7) in ischemic stroke.

Robert W Regenhardt, Fiona Desland, Adam P Mecca, David J Pioquinto, Aqeela Afzal, J Mocco, Colin Sumners

Abstract read
In one paragraph

Article in Neuropharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

70 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Renin-angiotensin system gene expression and neurodegenerative diseases.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2016
    Pooled it
  3. Article
  4. Review
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  9. Article
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  13. Article
  14. The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  15. Review
  16. Article
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  18. Review
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  20. Review

10 more citing papers are in PubMed but not listed here.

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

7 authors.

Robert W RegenhardtDepartment of Physiology and Functional Genomics, University of Florida, Gainesville, FL, USA.
Fiona Desland
Adam P Mecca
David J Pioquinto
Aqeela Afzal
J Mocco
Colin Sumners

Funding

Multidisciplinary Training Program in HypertensionT32HL083810 · NHLBI · UNIVERSITY OF FLORIDA · PI WOOD, CHARLES E · 2007 to 2017
$2.5M
Cerebroprotection via viral-mediated gene delivery of angiotensin AT2 receptorsF30NS060335 · NINDS · UNIVERSITY OF FLORIDA · PI MECCA, ADAM PETER · 2008 to 2011
$141k
NHLBI NIH HHS T32 HL-083810NHLBI NIH HHS T32 HL083810NINDS NIH HHS F30 NS-060335NINDS NIH HHS F30 NS060335
6 · The paper itself

Abstract

Previously we demonstrated that central administration of angiotensin-(1-7) [Ang-(1-7)] into rats elicits significant cerebroprotection against ischemic stroke elicited by endothelin-1 induced middle cerebral artery occlusion. Ang-(1-7), acting via its receptor Mas, reduced cerebral infarct size, and rats exhibited improved performance on neurological exams. These beneficial actions of Ang-(1-7) were not due to inhibition of the effects of endothelin-1 on cerebral vasoconstriction or effects on cerebral blood flow, and so we considered other potential mechanisms. Here we investigated the possibility that the Ang-(1-7)-induced cerebroprotection involves an anti-inflammatory effect, since stroke-induced cerebral damage includes an excessive intracerebral inflammatory response. Our quantitative RT-PCR analyses revealed that central Ang-(1-7) treatment attenuates the increased expression of mRNAs for inducible nitric oxide synthase (iNOS), several pro-inflammatory cytokines and cluster of differentiation molecule 11b (microglial marker) within the cerebral cortex following endothelin-1 induced stroke. Western blotting confirmed similar changes in iNOS protein expression in the cerebral cortex. In support of these observations, immunostaining revealed the presence of immunoreactive Mas on activated microglia within the cerebral cortical infarct zone, and in vitro experiments demonstrated that lipopolysaccharide-induced increases in nitric oxide production in glial cultures are attenuated by Ang-(1-7) acting via Mas. Collectively these findings demonstrate an anti-inflammatory action of Ang-(1-7) in the brain, and suggest that the cerebroprotective action of this peptide in ischemic stroke may involve effects on nitric oxide generation by microglia.

Indexed as

Angiotensin IAnimalsAnti-Inflammatory Agents, Non-SteroidalBrain IschemiaCells, CulturedCerebral CortexDisease Models, AnimalGene Expression RegulationMaleMiceMice, Inbred StrainsMice, KnockoutMicrogliaNerve Tissue ProteinsNeuroprotective AgentsNitric OxideAngiotensin Iangiotensin I (1-7)Anti-Inflammatory Agents, Non-SteroidalNerve Tissue ProteinsNeuroprotective AgentsNitric OxideNitric Oxide Synthase Type IIPeptide FragmentsProto-Oncogene MasProto-Oncogene ProteinsReceptors, G-Protein-Coupled

Identifiers

PMID23583926
PMCPMC3664115

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Registered trials

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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.