Evidence map›Paper›PMID 34496750›Full record

ArticleMolecular medicine (Cambridge, Mass.)2021

MicroRNA regulation of the proliferation and apoptosis of Leydig cells in diabetes.

Li Hu, Shaochai Wei, Yuqi Wu, Shulin Li, Pei Zhu, Xiangwei Wang

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

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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

6 authors at 2 institutions in 1 country.

Li HuShenzhen University South China Hospital, Shenzhen University, Shenzhen, 518111, People's Republic of China.
Shaochai WeiDepartment of Physiology, Shantou University of Medical College, Shantou, 515041, People's Republic of China.
Yuqi WuDepartment of Urology & Carson International Cancer Center, Shenzhen University General Hospital & Shenzhen University Clinical Medical Academy Center, Shenzhen University, NO.1098, Xueyuan Road, Shenzhen University City, Nanshan District, Shenzhen, 518055, People's Republic of China.
Shulin LiDepartment of Urology & Carson International Cancer Center, Shenzhen University General Hospital & Shenzhen University Clinical Medical Academy Center, Shenzhen University, NO.1098, Xueyuan Road, Shenzhen University City, Nanshan District, Shenzhen, 518055, People's Republic of China.
Pei ZhuDepartment of Urology & Carson International Cancer Center, Shenzhen University General Hospital & Shenzhen University Clinical Medical Academy Center, Shenzhen University, NO.1098, Xueyuan Road, Shenzhen University City, Nanshan District, Shenzhen, 518055, People's Republic of China. zhupei@szu.edu.cn.
Xiangwei WangDepartment of Urology & Carson International Cancer Center, Shenzhen University General Hospital & Shenzhen University Clinical Medical Academy Center, Shenzhen University, NO.1098, Xueyuan Road, Shenzhen University City, Nanshan District, Shenzhen, 518055, People's Republic of China. winn0324@szu.edu.cn.ORCID 0000-0001-8108-4979
Shenzhen University · CNShantou University · CN

Funding

Science and Technology Innovation Commission Foundation of Shenzhen JCYJ20180305124827261Science and Technology Innovation Commission Foundation of Shenzhen JCYJ20190808141013454shenzhen key laboratory foundation ZDSYS20200811143757022
6 · The paper itself

Abstract

backgroundThe number of patients with diabetes is increasing worldwide. Diabetic testicular damage can cause spermiogenesis disorders and sexual dysfunction. We thus explored the role of miRNAs in diabetic testicular damage, and revealed that they could serve as effective prevention and treatment therapeutic targets.

methodsStreptozotocin (STZ) was used to generate a rat model of type 2 diabetes. Rat testicular tissues were used for miRNA and mRNA sequencing. Through bioinformatics analysis, we constructed an miRNA-mRNA diabetic testicular damage regulatory network and screened for key miRNAs. We also used Leydig cells to generate a diabetic cell model and detected the downstream target genes of miRNAs, secretion of testosterone, and proliferation and apoptotic levels to elucidate the role and mechanism of the selected miRNAs in diabetic testicular damage.

resultsUsing second-generation sequencing, we identified 19 differentially expressed miRNAs and 555 mRNAs in the testes of diabetic rats. Based on computational prediction of targets and negative regulation relationships, we constructed a miRNA-mRNA regulatory network, including 12 miRNAs and 215 mRNAs. KEGG enrichment analysis revealed that genes were more concentrated on the survival signalling pathway. Based on this, we screened 2 key miRNAs, miR-504 and miR-935. In vitro, glucose could induce an increase in miR-504 and miR-935, whereas a decrease in MEK5 and MEF2C in a dose-dependent manner. Overexpression of miR-504 and miR-935 led to the decreased expression of MEK5 and MEF2C, decreased proliferation rate of Leydig cells, increased apoptotic rate, and decreased secretion of testosterone. Whereas, knockdown of miR-504 and miR-935 displayed opposite tendencies.

conclusionsmiRNAs play important roles in diabetic testicular damage. miR-504 and miR-935 might regulate testicular damage through the classic survival pathway of MEK5-ERK5-MEF2C. Targeted inhibition of miR-504 and miR-935 could reverse the high-glucose-induced testicular complications, thus posing as a potential therapeutic approach in diabetic testicular injury.

Indexed as

AnimalsApoptosisComputational BiologyDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Disease Models, AnimalGene Expression ProfilingGene Expression RegulationGlucoseHigh-Throughput Nucleotide SequencingLeydig CellsMaleMicroRNAsRatsRNA InterferenceSignal TransductionGlucoseMicroRNAsTestosteroneDiabetes mellitusMAPK signalling pathwaySmall RNATesticular damageTestosterone

Identifiers

PMID34496750
PMCPMC8425090
OpenAlexW3198066098

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.