Differential expression of microRNAs in TM3 Leydig cells of mice treated with brain‐derived neurotrophic factor

Gao, Shan; Li, Chunjin; Xu, Ying; Chen, Shuxiong; Zhao, Yun; Lu, Ciyong; Jiang, Yanwen; Liu, Zhuo; Fan, Rong; Sun, Liting; Wang, Fengge; Zhu, Xiaonian; Zhang, Jing; Zhou, Xu

doi:10.1002/cbf.3283

Cited by 9 publications

(5 citation statements)

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“…Elucidating the mechanism of ZEN toxicity to humans and animals is of great clinical significance to prevent and treat ZEN. Recent studies have shown that the addition of reproductive hormones to TM3 cells affects the expression of miRNAs in TM3 Leydig cells [17]. Therefore, we speculate that miRNAs are involved in the regulation of ZEN toxicology after ZEN is exposed to TM3 cells.…”

Section: Discussionmentioning

confidence: 80%

“…The miRNA maturation process involved in the nuclear processing of primary miRNA by DROSHA, nuclear export of precursor miRNA (pre- miRNA) by exportin 5, and cytoplasmic processing of pre- miRNA by DICER [15]. Recent studies showed that the differential expression of miRNAs in mouse Leydig cells was discovered by the addition of the brain-derived neurotrophic factor and luteinizing hormone during the cultivation of TM3 cells [16,17]. These studies show that miRNAs may be involved in the regulation of hormones in certain physiological functions of mouse Leydig cells.…”

Section: Introductionmentioning

confidence: 99%

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Analysis of the miRNA Expression Profiles in the Zearalenone-Exposed TM3 Leydig Cell Line

Wang

et al. 2019

IJMS

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Zearalenone (ZEN), an important environmental pollutant, can cause serious harm to human and animal health. The aim of our study was to examine the effect of zearalenone (ZEN) on miRNA expression profiles in the mouse Leydig cell line (TM3 Leydig cell line) by miRNA sequencing. The effect of ZEN on the viability of TM3 Leydig cells was verified by Cell Counting Kit-8 (CCK-8). MiRNA sequencing was performed 24 h after the exposure of TM3 Leydig cells with 50 μmol/L of ZEN. Bioinformatics predicted the miRNA target genes, performed Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, and conducted miRNA-gene-pathway mapping to show the relationship between miRNA, the target gene, and the signalling pathway. The expression levels of miRNA and the miRNA target genes associated with ZEN toxicology were verified by quantitative real-time polymerase chain reaction. The miRNA sequencing revealed a significant change (p < 0.05) in the 197 miRNAs in the ZEN-treated and control groups, among which 86 were up-regulated and 111 were down-regulated. GO analysis of the target genes of these miRNAs indicated various biological functions. KEGG analysis showed that the predicted miRNA target genes were involved in signalling pathways, such as cancer, apoptosis, and oxidation, namely, the Ras signalling pathway, Rap1 signalling pathway, PI3K-AKT signalling pathway, Foxo signalling pathway, and AMPK signalling pathway. These results suggest that ZEN, as an estrogen-like toxin, is regulated by microRNAs. Our results can help to examine the toxicological effects of ZEN-regulated miRNAs on germ cells.

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Section: Discussionmentioning

confidence: 80%

Section: Introductionmentioning

confidence: 99%

Analysis of the miRNA Expression Profiles in the Zearalenone-Exposed TM3 Leydig Cell Line

Wang

et al. 2019

IJMS

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“…Indeed, a bioinformatics analysis of the small RNA sequencing results identified several miRNAs that were differentially regulated in the cortices of 1-month-old NexKO mice compared to controls ( Figure 2 A–I). Most of these miRNAs were previously linked to brain development, such as miR-10b-5p [ 87 , 89 ], miR-145a-5p [ 90 ], miR-221-5p [ 91 ], miR-29c-5p [ 92 ], miR-186-5p [ 93 ], miR-34b-5p [ 94 ], and miR-34c-5p [ 94 ].…”

Section: Resultsmentioning

confidence: 99%

“…To examine this possibility, we utilized next-generation sequencing (NGS) techniques, which revealed considerable alterations in the expression levels of several miRNAs of interest in NexKO mice compared to controls. Among these were several miRNAs that were previously linked to brain development, such as miR-10b-5p [ 87 , 89 ], miR-145a-5p [ 90 ], miR-221-5p [ 91 ], miR-29c-5p [ 92 ], miR-186-5p [ 93 ], miR-34b-5p [ 94 ], and miR-34c-5p [ 94 ].…”

Section: Discussionmentioning

confidence: 99%

Altered White Matter and microRNA Expression in a Murine Model Related to Williams Syndrome Suggests That miR-34b/c Affects Brain Development via Ptpru and Dcx Modulation

Grad

Nir

Levy

et al. 2022

Cells

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Williams syndrome (WS) is a multisystem neurodevelopmental disorder caused by a de novo hemizygous deletion of ~26 genes from chromosome 7q11.23, among them the general transcription factor II-I (GTF2I). By studying a novel murine model for the hypersociability phenotype associated with WS, we previously revealed surprising aberrations in myelination and cell differentiation properties in the cortices of mutant mice compared to controls. These mutant mice had selective deletion of Gtf2i in the excitatory neurons of the forebrain. Here, we applied diffusion magnetic resonance imaging and fiber tracking, which showed a reduction in the number of streamlines in limbic outputs such as the fimbria/fornix fibers and the stria terminalis, as well as the corpus callosum of these mutant mice compared to controls. Furthermore, we utilized next-generation sequencing (NGS) analysis of cortical small RNAs’ expression (RNA-Seq) levels to identify altered expression of microRNAs (miRNAs), including two from the miR-34 cluster, known to be involved in prominent processes in the developing nervous system. Luciferase reporter assay confirmed the direct binding of miR-34c-5p to the 3’UTR of PTPRU—a gene involved in neural development that was elevated in the cortices of mutant mice relative to controls. Moreover, we found an age-dependent variation in the expression levels of doublecortin (Dcx)—a verified miR-34 target. Thus, we demonstrate the substantial effect a single gene deletion can exert on miRNA regulation and brain structure, and advance our understanding and, hopefully, treatment of WS.

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“…ZEA and its metabolites have structural analogy to estrogen, thus they can bind to estrogen receptors (ERs) and exert the estrogen-like effects [41]. Recent studies have shown that the addition of reproductive hormones including estrogen could affect the expression of miRNAs in TM3 Leydig cells [42]. Furthermore, study has clearly shown that oxidative stress can be a regulator of miRNAs, and can affect the expression of Micro-RNAs [43].…”

Section: Discussionmentioning

confidence: 99%

The Role of miRNAs in Zearalenone-Promotion of TM3 Cell Proliferation

Zheng

Fan

Feng

et al. 2019

IJERPH

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Zearalenone (ZEA) is a non-steroidal estrogen mycotoxin produced by several Gibberella and Fusarium species. Accumulating evidence has indicated that ZEA strongly stimulates cell proliferation. However the detailed molecular and cellular mechanisms of ZEA-mediated induction of cell proliferation have not yet been completely explained. The aim of this study was to detect the role of miRNAs in ZEA-mediated induction of cell proliferation. The effects of ZEA on cell proliferation were assessed using a cell counting kit assay and xCELLigence system. Micro-RNA sequencing was performed after treatment of TM3 cells with ZEA (0.01 μmol/L) for different time periods (0, 2, 6 and 18 h). Cell function and pathway analysis of the miRNA target genes were performed by Ingenuity Pathway Analysis (IPA). We found that ZEA promotes TM3 cell proliferation at low concentrations. miRNA sequenceing revealed 66 differentially expressed miRNAs in ZEA-treated cells in comparison to the untreated control ( p < 0.05). The miRNA sequencing indicated that compared to control group, there were 66 miRNAs significant change (p < 0.05) in ZEA-treated groups. IPA analysis showed that the predicated miRNAs target gene involved in cell Bio-functions including cell cycle, growth and proliferation, and in signaling pathways including MAPK and RAS-RAF-MEK-ERK pathways. Results from flow cytometry and Western Blot analysis validated the predictions that ZEA can affect cell cycle, and the MAPK signaling pathway. Taking these together, the cell proliferation induced ZEA is regulated by miRNAs. The results shed light on the molecular and cellular mechanisms for the mediation of ZEA to induce proliferation.

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Differential expression of microRNAs in TM3 Leydig cells of mice treated with brain‐derived neurotrophic factor

Cited by 9 publications

References 50 publications

Analysis of the miRNA Expression Profiles in the Zearalenone-Exposed TM3 Leydig Cell Line

Analysis of the miRNA Expression Profiles in the Zearalenone-Exposed TM3 Leydig Cell Line

Altered White Matter and microRNA Expression in a Murine Model Related to Williams Syndrome Suggests That miR-34b/c Affects Brain Development via Ptpru and Dcx Modulation

The Role of miRNAs in Zearalenone-Promotion of TM3 Cell Proliferation

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