Evidence map›Paper›PMID 26987907›Full record

ArticleScientific reports2016

Restoration of normal embryogenesis by mitochondrial supplementation in pig oocytes exhibiting mitochondrial DNA deficiency.

Gael L M Cagnone, Te-Sha Tsai, Yogeshwar Makanji, Pamela Matthews, Jodee Gould, Michael S Bonkowski, Kirstin D Elgass, Ashley S A Wong, Lindsay E Wu, Matthew McKenzie and 2 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 83 citations in OpenAlex.

  1. Review
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  10. Ovarian aging: energy metabolism of oocytes.Journal of ovarian research · 2024
    Review
  11. The role of mtDNA in oocyte quality and embryo development.Molecular reproduction and development · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Mitochondrial DNA Deficiency and Supplementation inInternational journal of molecular sciences · 2023
    Article
  16. Article
  17. Article
  18. Article
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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

12 authors at 4 institutions in 2 countries.

Gael L M CagnoneCentre for Genetic Diseases, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton, Vic 3168, Australia.
Te-Sha TsaiCentre for Genetic Diseases, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton, Vic 3168, Australia.
Yogeshwar MakanjiCentre for Genetic Diseases, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton, Vic 3168, Australia.
Pamela MatthewsCentre for Genetic Diseases, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton, Vic 3168, Australia.
Jodee GouldDepartment of Molecular and Translational Science, Monash University, 27-31 Wright Street, Clayton, Vic 3168, Australia.
Michael S BonkowskiDepartment of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA, 02115, USA.
Kirstin D ElgassMonash Micro Imaging, Monash University, 27-31 Wright Street, Vic 3168 Clayton, Australia.
Ashley S A WongSchool of Medical Sciences, University of New South Wales, NSW 2052, Australia.
Lindsay E WuSchool of Medical Sciences, University of New South Wales, NSW 2052, Australia.
Matthew McKenzieCentre for Genetic Diseases, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton, Vic 3168, Australia.
David A SinclairDepartment of Genetics, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA, 02115, USA.
Justin C St JohnCentre for Genetic Diseases, Hudson Institute of Medical Research, 27-31 Wright Street, Clayton, Vic 3168, Australia.
Hudson Institute of Medical Research · AUMonash University · AUHarvard University · USUNSW Sydney · AU

Funding

SIRT1 as a regulator of health and lifespan of mammalsR37AG028730 · NIA · HARVARD MEDICAL SCHOOL · PI SINCLAIR, DAVID A. · 2012 to 2021
$4.1M
NIA NIH HHS R37 AG028730
6 · The paper itself

Abstract

An increasing number of women fail to achieve pregnancy due to either failed fertilization or embryo arrest during preimplantation development. This often results from decreased oocyte quality. Indeed, reduced mitochondrial DNA copy number (mitochondrial DNA deficiency) may disrupt oocyte quality in some women. To overcome mitochondrial DNA deficiency, whilst maintaining genetic identity, we supplemented pig oocytes selected for mitochondrial DNA deficiency, reduced cytoplasmic maturation and lower developmental competence, with autologous populations of mitochondrial isolate at fertilization. Supplementation increased development to blastocyst, the final stage of preimplantation development, and promoted mitochondrial DNA replication prior to embryonic genome activation in mitochondrial DNA deficient oocytes but not in oocytes with normal levels of mitochondrial DNA. Blastocysts exhibited transcriptome profiles more closely resembling those of blastocysts from developmentally competent oocytes. Furthermore, mitochondrial supplementation reduced gene expression patterns associated with metabolic disorders that were identified in blastocysts from mitochondrial DNA deficient oocytes. These results demonstrate the importance of the oocyte's mitochondrial DNA investment in fertilization outcome and subsequent embryo development to mitochondrial DNA deficient oocytes.

Indexed as

Embryonic DevelopmentAnimalsBlastocystCulture MediaDNA Copy Number VariationsDNA, MitochondrialEmbryo Culture TechniquesFemaleFertilization in VitroGene Expression ProfilingMitochondriaOocytesPregnancySus scrofaSwineCulture MediaDNA, Mitochondrial

Identifiers

PMID26987907
PMCPMC4796791
OpenAlexW2322348567

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.