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MicroRNA‑30a‑5p regulates cypermethrin-induced apoptosis of Sertoli cells by targeting KLF9 in vitro.
- Source :
-
Reproductive Toxicology . Aug2023, Vol. 119, pN.PAG-N.PAG. 1p. - Publication Year :
- 2023
-
Abstract
- Cypermethrin (CYP) has been identified as one kind of endocrine-disrupting chemicals (EDCs) to induce male reproduction damage. This study aimed to investigate the effects and mechanisms of miR-30a-5p on CYP induced apoptosis of TM4 mouse Sertoli cells in vitro. In the present study, 0 μM, 10 μM, 20 μM, 40 μM and 80 μM CYP were used to treat TM4 cells for 24 h. The apoptosis of TM4 cells, the expression level of miR-30a-5p, the protein expressions and the interaction between miR-30a-5p and KLF9 were detected by flow cytometry, quantitative Real-Time PCR, Western blot and luciferase reporter assays. CYP induced apoptosis of TM4 cells, inhibited expression of miR-30a-5p in TM4 cells, and overexpression of miR-30a-5p partially recovered CYP induced cells apoptosis. Furthermore, KLF9 was a potential downstream target of miR-30a-5p predicted by publicly available databases. KLF9 expression level in TM4 cells was significantly elevated after treatment with CYP, and the induction was inhibited by miR-30a-5p mimics transfection. Meanwhile, dual-luciferase reporter assay demonstrated that miR-30a-5p directly targeted KLF9–3′UTR. Moreover, in the presence of CYP, the apoptosis regulator p53 expression was also increased in TM4 cells. Overexpression miR-30a-5p or down-regulation of KLF9 both attenuated the induction of CYP on p53 expression. Overall, the present study demonstrated that miR-30a-5p regulated CYP induced TM4 cells apoptosis by targeting KLF9/p53 axis. • miR-30a-5p regulated cypermethrin-induced apoptosis of TM4 cells. • KLF9 was a downstream target of miR-30a-5p. • miR-30a-5p regulated TM4 cells apoptosis by targeting KLF9/p53 axis. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 08906238
- Volume :
- 119
- Database :
- Academic Search Index
- Journal :
- Reproductive Toxicology
- Publication Type :
- Academic Journal
- Accession number :
- 164853974
- Full Text :
- https://doi.org/10.1016/j.reprotox.2023.108414