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miR-709 inhibits GHRP6 induced GH synthesis by targeting PRKCA in pituitary

文献类型： 外文期刊

作者： Cheng, Yunyun 1 ; Chen, Ting 1 ; Song, Jie 2 ; Qi, Qien 3 ; Wang, Chunli 2 ; Xi, Qianyun 1 ; Liu, Songcai 2 ; Hao, Linlin 2 ;

作者机构： 1.South China Agr Univ, Guangdong Prov Key Lab Anim Nutr Regulat, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Natl Engn Res Ctr Breeding Swine Ind,Coll Anim Sc, 483 Wushan Rd, Guangzhou 510642, Peoples R China

2.Jilin Univ, Coll Anim Sci, Jilin Prov Key Lab Anim Embryo Engn, 5333 Xian Roacl, Changchun 130062, Peoples R China

3.Foshan Univ, Sch Life Sci & Engn, Foshan 528231, Peoples R China

关键词： Pituitary; GH; miR-709; PKC alpha; GHRP6

期刊名称：MOLECULAR AND CELLULAR ENDOCRINOLOGY （ 影响因子：4.102； 五年影响因子：4.226 ）

ISSN： 0303-7207

年卷期： 2020 年 506 卷

页码：

收录情况： SCI

摘要： Pituitary growth hormone (GH) plays an essential role in processes of organism growth and metabolism. MicroRNA (miRNA) could also participate in diverse biological processes. However, the role of miRNA in the regulation of pituitary GH during the growth process remains unclear. In this study, we firstly confirmed that the second highly expressed pituitary miRNA (miR-709) significantly inhibited the GH synthesis and suppressed the viability of GH3 cells. The bioinformatics analysis and dual luciferase report system were used to ascertain the PRKCA is the direct target gene of miR-709, which is the coding gene of PKC alpha. Then the transcription and translation levels of Prkca were obvious reduced by the over-expression of miR-709 in GH3 cells, followed by the inhibition of the transcription factor (CREB1) of Ghl gene and the ERK1/2 signaling pathway or the possible cross-talk signaling pathway (cAMP/PKA signaling pathway) detected by western blot, suggesting that ERK1/2 maybe an important factor involved in the GH3 cell viability mediated by PKC alpha. At last, GHRP6 increased PKC alpha and GH expression but reduced miR-709 expression in vitro and vivo assays, and this conclusion was further confirmed by the result of GHRP6 attenuated the inhibition of miR-709 on GH expression. These findings will provide new molecular mechanism on the regulation of pituitary GH.

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