MiR-125b-2 Knockout in Testis Are Associated with Targeting to PAP Gene, Mitochondrial Copy Number and Impaired Sperm Quality

Li, Longlong; Zhu, Yanling; Sun, Jiajie; Chen, Ting; Luo, Junyi; Shu, Gang; Wang, Songbo; Zhu, Xiaotong; Jiang, Qingyan; Zhang, Yongliang; Xi, Qianyun

doi:10.20944/preprints201811.0563.v1

Cited by 2 publications

(2 citation statements)

References 29 publications

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“…The GC-2 spermatocyte cells were transfected for studying the function of the miRNA-450b-3p in these cells after exposure to the SiNPs. The present results showed that SiNPs downregulated the expression of (31) demonstrated that miR-125b-2 regulated testosterone secretions by targeting Papolb, and increased the DNA copy number of sperm mitochondria to in uence the semen quality. In male mice, miR-34b/c and − 449a/b/c led to sperm aggregation and agglutination, luminal obstruction, and sperm granulomas in male mice (32).…”

Section: Discussionsupporting

confidence: 51%

Silica nanoparticles inducing the apoptosis of spermatocyte cell through microRNA-450b-3p targeting MTCH2-mediating mitochondrial signaling pathway

Zhou

Liu

et al. 2020

Preprint

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Background: Silica nanoparticles (SiNPs) are found in environmental particulate matter and are proven to have adverse effects on fertility. The relationship and underlying mechanisms between miRNAs and apoptosis induced by SiNPs during spermatogenesis is currently ambiguous. Experimental design: The present study was designed to investigate the role of miRNA-450b-3p in the reproductive toxicity caused by SiNPs. In vivo, 40 male mice were randomly divided into control and SiNPs groups, 20 per group. The mice in the SiNPs group were administrated 20 mg/kg SiNPs by tracheal perfusion once every 5 days, for 35 days, and the control group were given the equivalent of a normal luminal saline. In vitro, spermatocyte cells were divided into 0 and 5 μg/mL SiNPs groups, after passaged for 30 generations, the GC-2spd cells in 5 μg/mL SiNPs groups were transfected with miRNA-450b-3p and its mimic and inhibitor. Results: In vivo, the results showed that SiNPs damaged tissue structures of testis, decreased the quantity and quality of the sperm, reduced the expression of miR-450b-3p, and increased the protein expressions of the MTCH2, BID, BAX, Cytochrome C, Caspase-9, and Caspase-3 in the testis. In vitro, SiNPs obviously repressed the viability and increased the LDH level and apoptosis rate, decreased the levels of the miR-450b-3p, significantly enhanced the protein expressions of the MTCH2, BID, BAX, Cytochrome C, Caspase-9, Caspase-3; while the mimic of miR-450b-3p reversed the changes induced by SiNPs, but inhibitor further promoted the effects induced by SiNPs.Conclusion: The result suggested that SiNPs could induce the spermatocyte apoptosis by inhibiting the miR-450b-3p expression to target promoting the MTCH2 resulting in activating mitochondrial apoptotic signaling pathways in the spermatocyte cells.

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Section: Discussionsupporting

confidence: 51%

Silica nanoparticles inducing the apoptosis of spermatocyte cell through microRNA-450b-3p targeting MTCH2-mediating mitochondrial signaling pathway

Zhou

Liu

et al. 2020

Preprint

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“…13 Evidence has shown that some miRNAs are abundantly expressed in various type of male germ cells. 14 Abu-Halima et al found that the level of miR-200a was notably upregulated in patients with different spermatogenic impairments. 15 However, the mechanism by which miR-200a regulated spermatogenic impairments remains unclear.…”

Section: Introductionmentioning

confidence: 99%

<p>Downregulation of miR-200a Protects Mouse Leydig Cells Against Triptolide by Triggering Autophagy</p>

Miao

2020

DDDT

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Background MicroRNAs play important roles in testicular development and spermatogenesis. Previous research has indicated that the level of miR-200a was significantly upregulated in patients with different spermatogenic impairments. However, the mechanism by which miR-200a regulated spermatogenic impairments remains unclear. Methods Leydig cells were treated with triptolide (TP) to mimic spermatogenic impairments. CCK-8 and flow cytometry were used to detect the proliferation and apoptosis in Leydig cells, respectively. In addition, Western blot assay was used to examine ATG7, ATG5, p62 protein levels in MLTC-1 cells. Results TP dose-dependently upregulated the expression of miR-200a in MLTC-1 cells. In addition, TP inhibited the proliferation of MLTC-1 cells via inducing apoptosis and oxidative stress; however, these phenomena were notably reversed by miR-200a antagomir. Furthermore, luciferase reporter assay identified that ATG7 was the direct binding target of miR-200a. TP treatment markedly inhibited the activation of autophagy in MLTC-1 cells via inhibition of ATG7. Conversely, downregulation of miR-200a significantly induced autophagy in TP-treated MLTC-1 cells by activation of ATG7. Meanwhile, the cell protective effects of miR-200a against TP were reversed by autophagy inhibitor 3MA, indicating that autophagy plays an important role. Conclusion These results indicated that downregulation of miR-200a could protect MLTC-1 cells against TP by inducing autophagy. Therefore, miR-200a might serve as a new therapeutic target for the treatment of male hypogonadism.

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MiR-125b-2 Knockout in Testis Are Associated with Targeting to PAP Gene, Mitochondrial Copy Number and Impaired Sperm Quality

Cited by 2 publications

References 29 publications

Silica nanoparticles inducing the apoptosis of spermatocyte cell through microRNA-450b-3p targeting MTCH2-mediating mitochondrial signaling pathway

Silica nanoparticles inducing the apoptosis of spermatocyte cell through microRNA-450b-3p targeting MTCH2-mediating mitochondrial signaling pathway

<p>Downregulation of miR-200a Protects Mouse Leydig Cells Against Triptolide by Triggering Autophagy</p>

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