Evidence map›Paper›PMID 24492657›Full record

ArticleThe Journal of reproduction and development2014

The association of mitochondrial potential and copy number with pig oocyte maturation and developmental potential.

Seul-Ki Lee, Ming-Hui Zhao, Jung-Woo Kwon, Ying-Hua Li, Zi-Li Lin, Yong-Xun Jin, Nam-Hyung Kim, Xiang-Shun Cui

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in The Journal of reproduction and development, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03438812 (The Role of Dehydroepiandrosterone in the Maintenance of Mitochondrial Quality of Cumulus Cells in Poor Ovarian Responders), which is not on this map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
9.6field-weighted citation impact, top 2% 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.

NCT03438812 nacompletednot on this mapstarted 2017, after this paper: background citation

The Role of Dehydroepiandrosterone in the Maintenance of Mitochondrial Quality of Cumulus Cells in Poor Ovarian Responders

TypeinterventionalSponsorKaohsiung Veterans General Hospital.Ran2017 to 2019Enrolled66ConditionsPoor Responders, DehydroepiandrosteroneArmsdehydroepiandrosterone (DHEA)
3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 69 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Spatiotemporal Distribution and Function of Mitochondria in Oocytes.Reproductive sciences (Thousand Oaks, Calif.) · 2024
    Review
  7. Effect of Endometriosis on Cumulus ATP, Number of Mitochondria and Oocyte Maturity in Cumulus Oocyte Complex in Mice.Revista brasileira de ginecologia e obstetricia : revista da Federacao Brasileira das Sociedades de Ginecologia e Obstetricia · 2023
    Article
  8. The role of mtDNA in oocyte quality and embryo development.Molecular reproduction and development · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Polycystic ovary syndrome and mitochondrial dysfunction.Reproductive biology and endocrinology : RB&E · 2019
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

8 authors at 1 institution in 1 country.

Seul-Ki LeeDepartment of Animal Sciences, Chungbuk National University, Cheongju, 361-763, South Korea.
Ming-Hui Zhao
Jung-Woo Kwon
Ying-Hua Li
Zi-Li Lin
Yong-Xun Jin
Nam-Hyung Kim
Xiang-Shun Cui
Chungbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

ATP is critical for oocyte maturation, fertilization, and subsequent embryo development. Both mitochondrial membrane potential and copy number expand during oocyte maturation. In order to differentiate the roles of mitochondrial metabolic activity and mtDNA copy number during oocyte maturation, we used two inhibitors, FCCP (carbonyl cyanide p-(tri-fluromethoxy)phenyl-hydrazone) and ddC (2'3-dideoxycytidine), to deplete the mitochondrial membrane potential (Δφm) and mitochondrial copy number, respectively. FCCP (2000 nM) reduced ATP production by affecting mitochondrial Δφm, decreased the mRNA expression of Bmp15 (bone morphogenetic protein 15), and shortened the poly(A) tails of Bmp15, Gdf9 (growth differentiation factor 9), and Cyclin B1 transcripts. FCCP (200 and 2000 nM) also affected p34(cdc2) kinase activity. By contrast, ddC did not alter ATP production. Instead, ddC significantly decreased mtDNA copy number (P < 0.05). FCCP (200 and 2000 nM) also decreased extrusion of the first polar body, whereas ddC at all concentrations did not affect the ability of immature oocytes to reach metaphase II. Both FCCP (200 and 2000 nM) and ddC (200 and 2000 µM) reduced parthenogenetic blastocyst formation compared with untreated oocytes. However, these inhibitors did not affect total cell number and apoptosis. These findings suggest that mitochondrial metabolic activity is critical for oocyte maturation and that both mitochondrial metabolic activity and replication contribute to the developmental competence of porcine oocytes.

Indexed as

Adenosine TriphosphateAnimalsBlotting, WesternBone Morphogenetic Protein 15Carbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneCDC2 Protein KinaseCyclin B1DNA, MitochondrialEmbryonic DevelopmentFemaleGene DosageGrowth Differentiation Factor 9In Situ Nick-End LabelingMembrane Potential, MitochondrialMitochondriaOocytesAdenosine TriphosphateBone Morphogenetic Protein 15Carbonyl Cyanide p-TrifluoromethoxyphenylhydrazoneCDC2 Protein KinaseCyclin B1DNA, MitochondrialGrowth Differentiation Factor 9RNAZalcitabine

Identifiers

PMID24492657
PMCPMC3999391
OpenAlexW1982858056

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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.