Evidence map›Paper›PMID 32164721›Full record

ArticleCell communication and signaling : CCS2020

Knocking-out the Siah2 E3 ubiquitin ligase prevents mitochondrial NCX3 degradation, regulates mitochondrial fission and fusion, and restores mitochondrial function in hypoxic neurons.

Maria Josè Sisalli, Gaetano Ianniello, Claudia Savoia, Ornella Cuomo, Lucio Annunziato, Antonella Scorziello

Open access · goldAbstract readVideo-Audio Media
In one paragraph

Article in Cell communication and signaling : CCS, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Maria Josè SisalliDivision of Pharmacology, Department of Neuroscience, Reproductive and Dentistry Sciences, School of Medicine, Federico II University of Naples, Via S. Pansini 5, 80131, Naples, Italy.
Gaetano IannielloDivision of Pharmacology, Department of Neuroscience, Reproductive and Dentistry Sciences, School of Medicine, Federico II University of Naples, Via S. Pansini 5, 80131, Naples, Italy.
Claudia SavoiaDivision of Pharmacology, Department of Neuroscience, Reproductive and Dentistry Sciences, School of Medicine, Federico II University of Naples, Via S. Pansini 5, 80131, Naples, Italy.
Ornella CuomoDivision of Pharmacology, Department of Neuroscience, Reproductive and Dentistry Sciences, School of Medicine, Federico II University of Naples, Via S. Pansini 5, 80131, Naples, Italy.
Lucio AnnunziatoIRCCS SDN, Naples, Italy.
Antonella ScorzielloDivision of Pharmacology, Department of Neuroscience, Reproductive and Dentistry Sciences, School of Medicine, Federico II University of Naples, Via S. Pansini 5, 80131, Naples, Italy. scorziel@unina.it.
University of Naples Federico II · ITSDN Istituto di Ricerca Diagnostica e Nucleare · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNa

methodsTo answer these questions, after exposing cortical neurons from siah2 KO mice (siah2 -/-) to OGD and OGD/Reoxygenation, we monitored the changes in mitochondrial fusion and fission protein expression, mitochondrial membrane potential (ΔΨm), and mitochondrial calcium concentration ([Ca

resultsAs opposed to congenic wild-type neurons, in neurons from siah2-/- mice exposed to OGD, form factor (FF), an index of the complexity and branching aspect of mitochondria, and aspect ratio (AR), an index reflecting the "length-to-width ratio" of mitochondria, maintained low expression. In KO siah2 neurons exposed to OGD, downregulation of mitofusin 1 (Mfn1), a protein involved in mitochondrial fusion and upregulation of dynamin-related protein 1 (Drp1), a protein involved in the mitochondrial fission, were prevented. Furthermore, under OGD conditions, whereas [Ca

conclusionsCollectively, these findings indicate that hypoxia-induced SIAH2-E3 ligase activation influences mitochondrial fusion and fission, as well as function, by inducing NCX3 degradation. Video Abstract.

Indexed as

Hypoxia-Ischemia, BrainNeuronsAnimalsCell HypoxiaCells, CulturedMembrane Potential, MitochondrialMiceMice, KnockoutMitochondriaMitochondrial DynamicsMitochondrial ProteinsPrimary Cell CultureSodium-Calcium ExchangerUbiquitin-Protein LigasesMitochondrial ProteinsSiah2 protein, mouseSlc8a3 protein, mouseSodium-Calcium ExchangerUbiquitin-Protein LigasesHypoxiaMitochondriaNCX3, cortical neuronssiah2

Identifiers

PMID32164721
PMCPMC7066748
OpenAlexW3011939586

What OpenQuestion holds

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LicenceCC BY
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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.