Evidence map›Paper›PMID 31264311›Full record

ArticleCell proliferation2019

Aurora B prevents aneuploidy via MAD2 during the first mitotic cleavage in oxidatively damaged embryos.

Jiena Li, Siyao Ha, Zhiling Li, Yue Huang, En Lin, Wanfen Xiao

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-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

9 citing papers in PubMed, 15 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.

Jiena LiReproductive Center, The First Affiliated Hospital of Shantou University Medical College, Shantou University, Shantou, China.ORCID https://orcid.org/0000-0001-7661-6686
Siyao HaLaboratory for Reproductive Immunology, Hospital & Institute of Obstetrics & Gynecology, Fudan University Shanghai Medical College, Shanghai, China.ORCID https://orcid.org/0000-0003-4884-1194
Zhiling LiReproductive Center, The First Affiliated Hospital of Shantou University Medical College, Shantou University, Shantou, China.ORCID https://orcid.org/0000-0002-1467-0641
Yue HuangReproductive Center, The First Affiliated Hospital of Shantou University Medical College, Shantou University, Shantou, China.
En LinReproductive Center, The First Affiliated Hospital of Shantou University Medical College, Shantou University, Shantou, China.
Wanfen XiaoReproductive Center, The First Affiliated Hospital of Shantou University Medical College, Shantou University, Shantou, China.
Shantou University · CNShanghai Medical College of Fudan University · CN

Funding

Guangdong Provincial Science and Technology Project 2016A020218015National Natural Science Foundation of China 2014A030313482National Natural Science Foundation of China 81471522National Natural Science Foundation of China 81671536National Natural Science Foundation of China 81871223Natural Science Foundation of Guangdong Province
6 · The paper itself

Abstract

objectivesA high rate of chromosome aneuploidy is exhibited in in vitro fertilization (IVF)-derived embryos. Our previous experiments suggested that reactive oxygen species (ROS) can activate Mad2, a key protein in the spindle assembly checkpoint (SAC), and delay the first mitotic, providing time to prevent the formation of embryonic aneuploidy. We aimed to determine whether mitotic kinase Aurora B was involved in the SAC function to prevent aneuploidy in IVF-derived embryos. MATERIALS AND

methodsWe analysed aneuploidy formation and repair during embryo pre-implantation via 4',6-diamidino-2-phenylindole (DAPI) staining and karyotype analysis. We assessed Aurora B activation by immunofluorescence and investigated the effect of Aurora B inhibition on embryo injury-related variables, such as embryonic development, ROS levels, mitochondrial membrane potential and γH2AX-positive expression.

resultsWe observed the expression and phosphorylation of Thr232 in Aurora B in oxidative stress-induced zygotes. Moreover, inhibition of Aurora B caused chromosome mis-segregation, abnormal spindle structures, abnormal chromosome number and reduced expression of Mad2 in IVF embryos. Our results suggest that Aurora B causes mitotic arrest and participates in SAC via Mad2 and H3S10P, which is required for self-correction of aneuploidies.

conclusionsWe demonstrate here that oxidative stress-induced DNA damage triggers Aurora B-mediated activation of SAC, which prevents aneuploidy at the first mitotic cleavage in early mouse IVF embryos.

Indexed as

AneuploidyAnimalsAurora Kinase BChromosome SegregationDNA DamageEmbryo, MammalianFemaleHydrogen PeroxideMad2 ProteinsMaleMembrane Potential, MitochondrialMiceMitosisM Phase Cell Cycle CheckpointsOrganophosphatesOxidative Stress2-((3-((4-((5-(2-((3-fluorophenyl)amino)-2-oxoethyl)-1H-pyrazol-3-yl)amino)quinazolin-7-yl)oxy)propyl)(ethyl)amino)ethyl dihydrogen phosphateAurkb protein, mouseAurora Kinase BHydrogen PeroxideMad2l1 protein, mouseMad2 ProteinsOrganophosphatesQuinazolinesReactive Oxygen SpeciesAurora Bchromosome aneuploidin vitro fertilizationoxidative stressspindle

Identifiers

PMID31264311
PMCPMC6797512
OpenAlexW2953742333

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.