Upregulation of miR-33 Exacerbates Heat-Stress-Induced Apoptosis in Granulosa Cell and Follicular Atresia of Nile Tilapia (Oreochromis niloticus) by Targeting TGF beta 1I1

文献类型： 外文期刊

第一作者： Qiang, Jun

作者： Qiang, Jun;Tao, Fan-Yi;Lu, Qi-Si;He, Jie;Xu, Pao;Qiang, Jun;Xu, Pao

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关键词： Oreochromis niloticus; transforming growth factor-beta-induced transcript 1; miR-33; follicular development; apoptosis

期刊名称：GENES （ 影响因子：4.141； 五年影响因子：4.474 ）

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年卷期： 2022 年 13 卷 6 期

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收录情况： SCI

摘要： High temperature affects egg quality and increases follicular atresia in teleosts. The present study aimed to explore the regulated mechanism of ovary syndrome of Nile tilapia (Oreochromis niloticus) exposed to heat stress. To this end, we conducted histological and biochemical analyses and integrated miRNA-target gene analyses. The histochemical analyses confirmed that heat stress promoted the apoptosis of granulosa cell and therefore resulted in increased follicular atresia in the ovary. Heat stress led to the differential expression of multiple miRNAs (miR-27e, -27b-3p, -33, -34a -133a-5p, and -301b-5p). In a luciferase activity assay, miR-33 bound to the 3'-untranslated region (UTR) of the TGF beta 1I1 (transforming growth factor-(beta 1-induced transcript 1) gene and inhibited its expression. A TGF beta 1I1 gene signal was detected in the granulosa cells of Nile tilapia by immunohistochemical analysis. Up-regulation of the miR-33 of tilapia at 6 d and 12 d exposed to heat (34.5 degrees C +/- 0.5 degrees C) had significant down-regulation of the TGF beta 1I1 expression of the gene and protein in tilapia ovaries. An miRNA-target gene integrated analysis revealed that miR-33 and TGF beta 1I1 function in an apoptosis-related signal pathway. The signal transduction of the vascular endothelial growth factor (VEGF) family members VEGFA and its receptor (KDR) in the heat-stressed group decreased significantly compared with the control group. Transcript-levels of the Bax and Caspase-3 as apoptotic promotors were activated and Bcl-2 and Caspase-8 as apoptotic inhibitors were suppressed in the heat-stressed tilapia. These results suggest that heat stress increases the expression of miR-33, which targets TGF beta 1I1 and inhibits its expression, resulting in decreased levels of follicle-stimulating hormone and 17 beta-estradiol and increased apoptosis by suppressing VEGF signaling, eventually inducing follicular atresia. In conclusion, our results show that the miR-33/TGF beta 1I1 axis of Nile tilapia is involved in the follicular development of broodstock, and can suppress VEGF signaling to accelerate follicular atresia. Our findings demonstrate the suppressive role of miR-33 during oocyte development in Nile tilapia.

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