AC3缺失对小鼠MOE组织内相关因子及信号通路的影响

发布时间：2018-05-13 15:42

本文选题：腺苷酸环化酶 + 主要嗅觉表皮组织　；参考：《基因组学与应用生物学》2017年10期

【摘要】：腺苷酸环化酶3(Adenylate cyclase 3,AC3)是膜整合蛋白,可将ATP变成cAMP,使cAMP信号通路受损,进而导致嗅觉丧失。主要嗅觉表皮(main olfactory epithelium,MOE)组织是感知和传导嗅觉信号的重要器官,主要通过环磷酸腺苷cAMP、肌醇1,4,5-三磷酸(Inositol 1,4,5-trisphosphate,IP3)、刺猬(Hedgehog,Hh)等3个信号通路进行嗅觉信号转导。MOE组织中有AC2、AC3、AC4等表达,为探讨当AC3缺失时,AC2和AC4是否可以发挥AC3作用介导嗅觉信号转导;AC3缺失是否通过引起IP3和Hh信号通路的改变而介导cAMP信号通路,本研究拟选取AC3缺失的小鼠和野生型小鼠各4只,以小鼠的MOE组织为实验材料,利用实时荧光定量PCR(q PCR)技术检测小鼠MOE组织内的AC2、AC4;检测IP3信号通路中的ip3r1、calm1、calm2;检测Hh信号通路中的patched、smoothened、gli1和gli2等基因的表达情况。结果显示,AC3缺失的小鼠中AC3几乎无表达;和野生型小鼠相比,AC3缺失的小鼠MOE组织中AC2、AC4表达量均显著下降(p0.05),分别下调1倍和4倍;AC3缺失的小鼠IP3信号通路中的三磷酸肌醇Ⅰ型受体(type 1 inositol1,4,5-trisphosphate receptor,ip3r1)、calm1、calm2表达量均显著下降(p0.05),分别下调0.3倍、10倍及4倍;AC3缺失的小鼠Hh信号通路中patched、smoothened、gli1和gli2的表达量均显著下降(p0.05),分别下调0.4倍、10倍、10倍、4倍。因此,AC3缺失会导致cAMP信号通路的调节受损,进而影响AC3相关因子AC2和AC4的表达,同时抑制IP3和Hh信号通路的传导,在探究AC3基因敲出小鼠嗅觉丧失方面具有一定的指导意义。
[Abstract]:Adenylate cyclase (3(Adenylate cyclase _ 3 / AC3) is a membrane integrin, which can transform ATP into cAMPand damage cAMP signaling pathway and lead to olfactory loss. Main olfactory epithelium moe) is an important organ for sensing and transduction of olfactory signals. It is expressed mainly through three signal pathways of cyclic adenosine monophosphate (cAMPP), inositol (Inositol 1AMP4), Inositol 1( 4) trisphosphate5 (IP3) and Hedgehog (HH). To investigate whether AC2 and AC4 can mediate olfactory signal transduction by AC3 when AC3 is absent, whether cAMP signaling pathway is mediated by IP3 and Hh signaling pathway. In this study, 4 AC3 deficient mice and 4 wild-type mice were selected. The MOE tissues of mice were used as experimental materials. Real-time fluorescence quantitative PCR(q was used to detect AC2AC4 in mouse MOE tissue, ip3r1calm1calm1calm2 in IP3 signaling pathway, and the expression of patchededmenedtgli1 and gli2 genes in Hh signaling pathway. The results showed that there was almost no expression of AC3 in mice with AC3 deletion. Compared with wild-type mice, the expression of AC2mA4 in MOE of mice with ACA 3 deletion decreased significantly (p0.05), and the expression of inositol I receptor type 1 inositol I receptor ip3r1r1 calm1 calm2 was down-regulated in IP3 signaling pathway of mice with 1 and 4 times AC3 deletion, respectively. The expression of patchedad smooth edGlil 1 and gli2 in the Hh signaling pathway of mice with 0. 3 and 4 times of AC3 deletion decreased significantly (p0. 05), and decreased by 0. 4 times, 10 times and 4 times, respectively. Therefore, the deletion of AC3 may result in impaired regulation of cAMP signaling pathway, and then affect the expression of AC2 and AC4, and inhibit the transduction of IP3 and Hh signaling pathway, which has certain guiding significance in exploring the olfactory loss of AC3 knockout mice.
【作者单位】：海南医学院;海南省人民医院;
【分类号】：R339.12

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