Evidence map›Paper›PMID 25501014›Full record

ArticleThe Journal of reproduction and development2015

Mdivi-1, mitochondrial fission inhibitor, impairs developmental competence and mitochondrial function of embryos and cells in pigs.

Ji-Yeong Yeon, Sung-Hun Min, Hyo-Jin Park, Jin-Woo Kim, Yong-Hee Lee, Soo-Yong Park, Pil-Soo Jeong, Humdai Park, Dong-Seok Lee, Sun-Uk Kim and 2 more

Abstract read
In one paragraph

Article in The Journal of reproduction and development, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Players in Mitochondrial Dynamics and Female Reproduction.Frontiers in molecular biosciences · 2021
    Review
  4. Review
  5. Article
  6. Mitochondrial dynamics in exercise physiology.Pflugers Archiv : European journal of physiology · 2020
    Review
  7. Review
  8. Article
  9. CaMolecular metabolism · 2017
    Article
  10. Article
  11. The Emerging Role of Mitochondrial Targeting in Kidney Disease.Handbook of experimental pharmacology · 2017
    Review
  12. Review
  13. Review
  14. 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

12 authors.

Ji-Yeong YeonDepartment of Biotechnology, College of Engineering, Daegu University, Gyeongbuk 712-714, Republic of Korea.
Sung-Hun Min
Hyo-Jin Park
Jin-Woo Kim
Yong-Hee Lee
Soo-Yong Park
Pil-Soo Jeong
Humdai Park
Dong-Seok Lee
Sun-Uk Kim
Kyu-Tae Chang
Deog-Bon Koo

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are highly dynamic organelles that undergo constant fusion/fission as well as activities orchestrated by large dynamin-related GTPases. These dynamic mitochondrial processes influence mitochondrial morphology, size and function. Therefore, this study was conducted to evaluate the effects of mitochondrial fission inhibitor, mdivi-1, on developmental competence and mitochondrial function of porcine embryos and primary cells. Presumptive porcine embryos were cultured in PZM-3 medium supplemented with mdivi-1 (0, 10 and 50 μM) for 6 days. Porcine fibroblast cells were cultured in growth medium with mdivi-1 (0 and 50 μM) for 2 days. Our results showed that the rate of blastocyst production and cell growth in the mdivi-1 (50 μM) treated group was lower than that of the control group (P < 0.05). Moreover, loss of mitochondrial membrane potential in the mdivi-1 (50 μM) treated group was increased relative to the control group (P < 0.05). Subsequent evaluation revealed that the intracellular levels of reactive oxygen species (ROS) and the apoptotic index were increased by mdivi-1 (50 μM) treatment (P < 0.05). Finally, the expression of mitochondrial fission-related protein (Drp 1) was lower in the embryos and cells in the mdivi-1-treated group than the control group. Taken together, these results indicate that mdivi-1 treatment may inhibit developmental competence and mitochondrial function in porcine embryos and primary cells.

Indexed as

AnimalsApoptosisDeath-Associated Protein KinasesEmbryo Culture TechniquesEmbryonic DevelopmentMembrane Potential, MitochondrialMitochondriaMitochondrial DynamicsQuinazolinonesReactive Oxygen SpeciesSwine3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneDeath-Associated Protein KinasesQuinazolinonesReactive Oxygen Species

Identifiers

PMID25501014
PMCPMC4410306

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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.