LncRNA3215-ceRNA-miR1594调控肌钙蛋白T参与鸡缺硒性心肌细胞凋亡的作用研究

心肌是硒缺乏的靶器官之一。课题组前期应用组学技术发现，LncRNA-3215在鸡缺硒性心肌损伤过程中显著上调，其可能作用miR-1594显著下调，且预测共同靶基因为肌钙蛋白T（cTnT），但lncRNA是否可作为ceRNA参与miRNA调控cTnT及其在鸡缺硒性心肌损伤中的作用机制尚不清楚。.本课题在建立鸡缺硒性心肌损伤模型基础上，通过对心肌组织LncRNA-3215、miR-1594及细胞内钙稳态和细胞凋亡相关通路的检测，结合前期生物信息学结果，对靶基因cTnT进行鉴定并确定其在鸡缺硒性心肌细胞损伤中的可能信号转导通路，在此基础上通过体外培养鸡心肌细胞，分别建立LncRNA-3215、miR-1594抑制及过表达模型以及LncRNA-3215、cTnT基因过表达鸡胚模型，检测细胞内钙稳态及细胞凋亡相关通路，阐明LncRNA和miRNA调控网络在鸡缺硒性心肌损伤性凋亡中的作用机制。

Myocardium is one of the target organs of selenium deficiency. In our previous study, we found that LncRNA-3215 upregulated in chicken heart induced by Se deficiency by whole transcriptome resequencing.The possible related miR-1594 is significantly down-regulated. We also predict that their target gene is troponin T (cTnT). However, it is not clear whether LncRNA can act as ceRNA to participate in the regulation on cTnT by miRNA and its mechanism in Se-deficient myocardial injury in chickens still unclear.. Base on the cases model of myocardial damage induced by Se deficiency in chickens. To detect of LncRNA-3215, miR-1594, intracellular calcium homeostasis, apoptosis-related genes and proteins expression in myocardial tissue, combined with previous bioinformatics results to identify the target gene cTnT and the possible signal transduction pathways in Se-induced cardiomyocyte damage in chickens. On this basis, chicken cardiomyocytes were cultured in vitro to established LncRNA-3215 and miR-1594 inhibition and overexpression models and LncRNA-3215 and cTnT overexpressed chicken embryo models, respectively. To detect the intracellular calcium homeostasis, apoptosis-related genes and proteins expression in cardiomyocytes and chicken embryo models to illuminate the mechanism of LncRNA and miRNA regulatory networks in apoptosis in myocardial damage induced by selenium deficiency.