Evidence map›Paper›PMID 31162612›Full record

ArticleBiology of reproduction2019

Influence of mouse defective zona pellucida in folliculogenesis on apoptosis of granulosa cells and developmental competence of oocytes†.

Yan Wang, Chao Lv, Hua-Lin Huang, Ming-Hua Zeng, Da-Jing Yi, Hang-Jing Tan, Tian-Liu Peng, Wen-Xian Yu, Hong-Wen Deng, Hong-Mei Xiao

Open access · greenAbstract read
In one paragraph

Article in Biology of reproduction, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

10 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. True empty follicle syndrome is a subtype of oocyte maturation abnormalities.Turkish journal of obstetrics and gynecology · 2024
    Article
  5. A heterozygousiScience · 2023
    Article
  6. Article
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  8. Review
  9. Review
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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

10 authors at 2 institutions in 2 countries.

Yan WangInstitute of Reproductive and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Chao LvInstitute of Reproductive and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Hua-Lin HuangInstitute of Reproductive and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Ming-Hua ZengInstitute of Reproductive and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Da-Jing YiInstitute of Reproductive and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Hang-Jing TanInstitute of Reproductive and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Tian-Liu PengInstitute of Reproductive and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Wen-Xian YuInstitute of Reproductive and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Hong-Wen DengCenter of System Biology and Data Science, School of Basic Medical Science, Central South University, Changsha, China.
Hong-Mei XiaoInstitute of Reproductive and Stem Cell Engineering, School of Basic Medical Science, Central South University, Changsha, China.
Central South University · CNTulane University · US

Funding

Trans-omics Integration of Multi-omics Studies for OsteoporosisU19AG055373 · NIA · TULANE UNIVERSITY OF LOUISIANA · PI HUI SHEN · 2017 to 2026
$24.3M
Decoding Methylation Mediated Epigenomic Contributions to Male OsteoporosisR01AR069055 · NIAMS · TULANE UNIVERSITY OF LOUISIANA · PI DENG, HONG-WEN · 2017 to 2021
$2.9M
NIAMS NIH HHS R01 AR069055NIA NIH HHS U19 AG055373
6 · The paper itself

Abstract

Zona pellucida (ZP), which enwraps the oocyte during folliculogenesis, initially forms in the primary follicle and plays an important role in female fertility. Here, we investigated a mouse strain ("mutant mice" for short) carrying two types of ZP defects in folliculogenesis, i.e., ZP thinned (but intact) and ZP cracked, caused by targeted mutation in the Zp1 gene. Using this mutant mouse strain and wild-type mouse as control, we studied the effects of the ZP defects on the development of oocytes and granulosa cells during folliculogenesis. For each ZP defect, we examined the morphology of transzonal projections and apoptosis of granulosa cells in the corresponding growing follicles, as well as the morphology of corresponding ovulated eggs and their abilities to develop into viable individuals. Our results suggested that ZP integrity rather than thickness or porosity is crucial for preventing the ectopia of granulosa cells, maintaining adequate routine bilateral signaling between oocyte and surrounding granulosa cells, and thus for ensuring the survival of granulosa cells and the establishment of the full developmental competence of oocytes. This is the first study to elucidate the effects of different degrees of ZP defects caused by the same gene mutation, on the apoptosis of granulosa cells and developmental competence of oocytes, and to explore the potential mechanisms underlying these effects.

Indexed as

Amino Acid SequenceAnimalsApoptosisFemaleGene Expression RegulationGranulosa CellsMiceMutationOocytesZona PellucidaZona Pellucida GlycoproteinsZona Pellucida GlycoproteinsZp1 protein, mouseapoptosisblastocystembryo culturegranulosa cellsinfertilityoocyte developmentoocyte-follicle interactionszona pellucida

Identifiers

PMID31162612
PMCPMC8127037
OpenAlexW2948049014

What OpenQuestion holds

Textmetadata
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.