Evidence map›Paper›PMID 32854459›Full record

ArticleClinical and experimental reproductive medicine2020

miR-4463 regulates aromatase expression and activity for 17β-estradiol synthesis in response to follicle-stimulating hormone.

Su-Yeon Lee, Youn-Jung Kang, Jinie Kwon, Yoshihiro Nishi, Toshihiko Yanase, Kyung-Ah Lee, Mi Kyoung Koong

Open access · diamondAbstract read
In one paragraph

Article in Clinical and experimental reproductive medicine, 2020. 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
0.5field-weighted citation impact, top 37% 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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  6. The possible regulatory role of miR-4463 and its target geneInternational journal of reproductive biomedicine · 2024
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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

7 authors at 3 institutions in 2 countries.

Su-Yeon LeeDepartment of Biomedical Science, College of Life Science, Institute of Reproductive Medicine, CHA University, Seongnam, Korea.
Youn-Jung KangDepartment of Biomedical Science, College of Life Science, Institute of Reproductive Medicine, CHA University, Seongnam, Korea.
Jinie KwonDepartment of Biomedical Science, College of Life Science, Institute of Reproductive Medicine, CHA University, Seongnam, Korea.
Yoshihiro NishiDepartment of Physiology, Kurume University School of Medicine, Kurume, Japan.
Toshihiko YanaseDepartment of Endocrinology and Diabetes Mellitus, School of Medicine, Fukuoka University, Fukuoka, Japan.
Kyung-Ah LeeDepartment of Biomedical Science, College of Life Science, Institute of Reproductive Medicine, CHA University, Seongnam, Korea.
Mi Kyoung KoongDepartment of Obstetrics and Gynecology, CHA University, Fertility Center, CHA General Hospital, Seoul, Korea.
CHA University · KRFukuoka University · JPKurume University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe aim of this study was to investigate microRNAs (miRNAs) related to follicle-stimulating hormone (FSH) responsiveness using miRNA microarrays and to identify their target genes to determine the molecular regulatory pathways involved in FSH signaling in KGN cells.

methodsTo change the cellular responsiveness to FSH, KGN cells were treated with FSH receptor (FSHR)-specific small interfering RNA (siRNA) followed by FSH. miRNA expression profiles were determined through miRNA microarray analysis. Potential target genes of selected miRNAs were predicted using bioinformatics tools, and their regulatory function was confirmed in KGN cells.

resultsWe found that six miRNAs (miR-1261, miR-130a-3p, miR-329-3p, miR-185-5p, miR-144-5p and miR-4463) were differentially expressed after FSHR siRNA treatment in KGN cells. Through a bioinformatics analysis, we showed that these miRNAs were predicted to regulate a large number of genes, which we narrowed down to cytochrome P450 family 19 subfamily A member 1 (CYP19A1) and estrogen receptor alpha (ESR1) as the main targets for miR-4463. Functional analysis revealed that miR-4463 is a regulatory factor for aromatase expression and function in KGN cells.

conclusionIn this study, we identified differentially expressed miRNAs related to FSH responsiveness. In particular, upregulation of miR-4463 expression by FSHR deficiency in human granulosa cells impaired 17β-estradiol synthesis by targeting CYP19A1 and ESR1. Therefore, our data might provide novel candidates for molecular biomarkers for use in research into poor responders.

Indexed as

CYP19A1 protein, humanESR1 protein, humanHsa-mir-4463

Identifiers

PMID32854459
PMCPMC7482943
OpenAlexW3082494508

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Registered trials

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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.