Evidence map›Paper›PMID 22397398›Full record

ArticleJournal of neuroinflammation2012

Regulator of calcineurin 1 (Rcan1) has a protective role in brain ischemia/reperfusion injury.

Mónica Sobrado, Belén G Ramirez, Fernando Neria, Ignacio Lizasoain, Maria Lourdes Arbones, Takashi Minami, Juan Miguel Redondo, María Angeles Moro, Eva Cano

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

39 citing papers in PubMed, 59 citations in OpenAlex.

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  14. Spatiotemporal expression of RCAN1 and its isoformThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2020
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  19. Down Syndrome Critical Region 1 Gene,Circulation research · 2018
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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

9 authors at 6 institutions in 2 countries.

Mónica SobradoUnidad de Investigación Neurovascular, Departamento de Farmacología, Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain.
Belén G Ramirez
Fernando Neria
Ignacio Lizasoain
Maria Lourdes Arbones
Takashi Minami
Juan Miguel Redondo
María Angeles Moro
Eva Cano
Universidad Complutense de Madrid · ESSpanish National Centre for Cardiovascular Research · ESCentre for Biomedical Network Research on Rare Diseases · ESCentro Nacional de Microbiologia · ESInstituto de Salud Carlos III · ESThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAn increase in intracellular calcium concentration [Ca2+]i is one of the first events to take place after brain ischemia. A key [Ca2+]i-regulated signaling molecule is the phosphatase calcineurin (CN), which plays important roles in the modulation of inflammatory cascades. Here, we have analyzed the role of endogenous regulator of CN 1 (Rcan1) in response to experimental ischemic stroke induced by middle cerebral artery occlusion.

methodsAnimals were subjected to focal cerebral ischemia with reperfusion. To assess the role of Rcan1 after stroke, we measured infarct volume after 48 h of reperfusion in Rcan1 knockout (KO) and wild-type (WT) mice. In vitro studies were performed in astrocyte-enriched cortical primary cultures subjected to 3% oxygen (hypoxia) and glucose deprivation (HGD). Adenoviral vectors were used to analyze the effect of overexpression of Rcan1-4 protein. Protein expression was examined by immunohistochemistry and immunoblotting and expression of mRNA by quantitative real-time Reverse-Transcription Polymerase Chain Reaction (real time qRT-PCR).

resultsBrain ischemia/reperfusion (I/R) injury in vivo increased mRNA and protein expression of the calcium-inducible Rcan1 isoform (Rcan1-4). I/R-inducible expression of Rcan1 protein occurred mainly in astroglial cells, and in an in vitro model of ischemia, HGD treatment of primary murine astrocyte cultures induced Rcan1-4 mRNA and protein expression. Exogenous Rcan1-4 overexpression inhibited production of the inflammatory marker cyclo-oxygenase 2. Mice lacking Rcan1 had higher expression of inflammation associated genes, resulting in larger infarct volumes.

conclusionsOur results support a protective role for Rcan1 during the inflammatory response to stroke, and underline the importance of the glial compartment in the inflammatory reaction that takes place after ischemia. Improved understanding of non-neuronal mechanisms in ischemic injury promises novel approaches to the treatment of acute ischemic stroke.

Indexed as

Analysis of VarianceAnimalsAnimals, NewbornAstrocytesBrainBrain InfarctionCalcium-Binding ProteinsCell HypoxiaCells, CulturedCerebral CortexCyclooxygenase 2CytokinesDisease Models, AnimalGene Expression RegulationGlial Fibrillary Acidic ProteinGlucosecalcineurin phosphataseCalcium-Binding ProteinsCyclooxygenase 2CytokinesDSCR1 protein, mouseGlial Fibrillary Acidic ProteinGlucoseIntracellular Signaling Peptides and ProteinsMuscle ProteinsPhosphoric Monoester HydrolasesRCAN1 protein, ratRNA, Messenger

Identifiers

PMID22397398
PMCPMC3325863
OpenAlexW2149674371

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.