Evidence map›Paper›PMID 32492799›Full record

ArticleCells2020

A Role for mir-26a in Stress: A Potential sEV Biomarker and Modulator of Excitatory Neurotransmission.

Carlos Andrés Lafourcade, Anllely Fernández, Juan Pablo Ramírez, Katherine Corvalán, Miguel Ángel Carrasco, Andrés Iturriaga, Luis Federico Bátiz, Alejandro Luarte, Ursula Wyneken

Open access · goldAbstract read
In one paragraph

Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Gm26550 Modulates Learning and Memory by Increasing IGF1 mRNA Expression and Stability in Nrf2Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 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

9 authors at 2 institutions in 1 country.

Carlos Andrés LafourcadeCentro de Investigación e Innovación Biomédica (CIIB), Facultad de Medicina, Universidad de los Andes, Santiago PC 7620001, Chile.
Anllely FernándezCentro de Investigación e Innovación Biomédica (CIIB), Facultad de Medicina, Universidad de los Andes, Santiago PC 7620001, Chile.
Juan Pablo RamírezCentro de Investigación e Innovación Biomédica (CIIB), Facultad de Medicina, Universidad de los Andes, Santiago PC 7620001, Chile.
Katherine CorvalánCentro de Investigación e Innovación Biomédica (CIIB), Facultad de Medicina, Universidad de los Andes, Santiago PC 7620001, Chile.
Miguel Ángel CarrascoFacultad de Ingeniería y Ciencias Aplicadas, Universidad de los Andes, Santiago PC 7620001, Chile.
Andrés IturriagaInstituto de Salud Poblacional, Facultad de Medicina, Universidad de Chile, Santiago PC 8380453, Chile.
Luis Federico BátizCentro de Investigación e Innovación Biomédica (CIIB), Facultad de Medicina, Universidad de los Andes, Santiago PC 7620001, Chile.ORCID 0000-0002-3043-8797
Alejandro LuarteBiomedical Neuroscience Institute, Universidad de Chile, Santiago PC 8380453, Chile.ORCID 0000-0001-9138-1854
Ursula WynekenCentro de Investigación e Innovación Biomédica (CIIB), Facultad de Medicina, Universidad de los Andes, Santiago PC 7620001, Chile.
Universidad de Los Andes, Chile · CLUniversity of Chile · CL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Stress is a widespread problem in today's societies, having important consequences on brain function. Among the plethora of mechanisms involved in the stress response at the molecular level, the role of microRNAs (miRNAs) is beginning to be recognized. The control of gene expression by these noncoding RNAs makes them essential regulators of neuronal and synaptic physiology, and alterations in their levels have been associated with pathological conditions and mental disorders. In particular, the excitatory (i.e., glutamate-mediated) neurotransmission is importantly affected by stress. Here, we found that loss of miR-26a-5p (miR-26a henceforth) function in primary hippocampal neurons increased the frequency and amplitude of miniature excitatory currents, as well as the expression levels of the excitatory postsynaptic scaffolding protein PSD95. Incubation of primary hippocampal neurons with corticosterone downregulated miR-26a, an effect that mirrored our in vivo results, as miR-26a was downregulated in the hippocampus as well as in blood serum-derived small extracellular vesicles (sEVs) of rats exposed to two different stress paradigms by movement restriction (i.e., stress by restraint in cages or by complete immobilization in bags). Overall, these results suggest that miR-26a may be involved in the generalized stress response and that a stress-induced downregulation of miR-26a could have long-term effects on glutamate neurotransmission.

Indexed as

Synaptic TransmissionAnimalsBiomarkersDisease Models, AnimalDisks Large Homolog 4 ProteinDown-RegulationExtracellular VesiclesMicroRNAsMiniature Postsynaptic PotentialsRats, Sprague-DawleyStress, PsychologicalSynapsesBiomarkersDisks Large Homolog 4 ProteinMicroRNAsMIRN26 microRNA, ratextracellular vesicleshippocampal neuronsmiRNAsstresssynapses

Identifiers

PMID32492799
PMCPMC7349773
OpenAlexW3029980035

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.