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miR-709 inhibits GHRP6 induced GH synthesis by targeting PRKCA in pituitary.
Molecular and Cellular Endocrinology ( IF 3.8 ) Pub Date : 2020-02-19 , DOI: 10.1016/j.mce.2020.110763 Yunyun Cheng 1 , Ting Chen 1 , Jie Song 2 , Qien Qi 3 , Chunli Wang 2 , Qianyun Xi 1 , Songcai Liu 2 , Linlin Hao 2 , Yongliang Zhang 1
Molecular and Cellular Endocrinology ( IF 3.8 ) Pub Date : 2020-02-19 , DOI: 10.1016/j.mce.2020.110763 Yunyun Cheng 1 , Ting Chen 1 , Jie Song 2 , Qien Qi 3 , Chunli Wang 2 , Qianyun Xi 1 , Songcai Liu 2 , Linlin Hao 2 , Yongliang Zhang 1
Affiliation
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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 PKCα. 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 Gh1 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 PKCα. At last, GHRP6 increased PKCα 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.
中文翻译：
miR-709通过靶向垂体中的PRKCA抑制GHRP6诱导的GH合成。
垂体生长激素（GH）在生物体生长和代谢过程中起重要作用。MicroRNA（miRNA）也可以参与多种生物学过程。然而，在生长过程中，miRNA在垂体生长激素调节中的作用尚不清楚。在这项研究中，我们首先证实第二个高度表达的垂体miRNA（miR-709）显着抑制GH的合成并抑制GH3细胞的生存能力。通过生物信息学分析和双重荧光素酶报告系统确定PRCAA是miR-709的直接靶基因，miR-709是PKCα的编码基因。然后miR-709在GH3细胞中的过表达明显降低了Prkca的转录和翻译水平，其次是抑制Gh1基因的转录因子（CREB1）和ERK1 / 2信号通路或通过蛋白质印迹检测到的可能的串扰信号通路（cAMP / PKA信号通路），提示ERK1 / 2可能是一个重要因素参与由PKCα介导的GH3细胞活力。最终，GHRP6在体外和体内试验中增加了PKCα和GH的表达，但降低了miR-709的表达，GHRP6的结果减弱了miR-709对GH表达的抑制作用，进一步证实了这一结论。这些发现将为垂体GH的调控提供新的分子机制。GHRP6在体外和体内试验中增加了PKCα和GH的表达，但降低了miR-709的表达，GHRP6的结果减弱了miR-709对GH表达的抑制作用，进一步证实了这一结论。这些发现将为垂体GH的调控提供新的分子机制。GHRP6在体外和体内试验中增加了PKCα和GH的表达，但降低了miR-709的表达，GHRP6的结果减弱了miR-709对GH表达的抑制作用，进一步证实了这一结论。这些发现将为垂体GH的调控提供新的分子机制。
更新日期：2020-02-20
中文翻译：
miR-709通过靶向垂体中的PRKCA抑制GHRP6诱导的GH合成。
垂体生长激素（GH）在生物体生长和代谢过程中起重要作用。MicroRNA（miRNA）也可以参与多种生物学过程。然而，在生长过程中，miRNA在垂体生长激素调节中的作用尚不清楚。在这项研究中，我们首先证实第二个高度表达的垂体miRNA（miR-709）显着抑制GH的合成并抑制GH3细胞的生存能力。通过生物信息学分析和双重荧光素酶报告系统确定PRCAA是miR-709的直接靶基因，miR-709是PKCα的编码基因。然后miR-709在GH3细胞中的过表达明显降低了Prkca的转录和翻译水平，其次是抑制Gh1基因的转录因子（CREB1）和ERK1 / 2信号通路或通过蛋白质印迹检测到的可能的串扰信号通路（cAMP / PKA信号通路），提示ERK1 / 2可能是一个重要因素参与由PKCα介导的GH3细胞活力。最终，GHRP6在体外和体内试验中增加了PKCα和GH的表达，但降低了miR-709的表达，GHRP6的结果减弱了miR-709对GH表达的抑制作用，进一步证实了这一结论。这些发现将为垂体GH的调控提供新的分子机制。GHRP6在体外和体内试验中增加了PKCα和GH的表达，但降低了miR-709的表达，GHRP6的结果减弱了miR-709对GH表达的抑制作用，进一步证实了这一结论。这些发现将为垂体GH的调控提供新的分子机制。GHRP6在体外和体内试验中增加了PKCα和GH的表达，但降低了miR-709的表达，GHRP6的结果减弱了miR-709对GH表达的抑制作用，进一步证实了这一结论。这些发现将为垂体GH的调控提供新的分子机制。
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