文献类型：期刊文献

英文题名：Chicken GHR antisense transcript regulates its sense transcript in hepatocytes

作者：Wang, Zhang[1];Xu, HaiDong[1];Li, Ting[1];Wu, Jiang[1];An, LiLong[1];Zhao, ZhiHui[1];Xiao, Mei[1];Adu-Asiamah, Patricia[1];Zhang, XiQuan[2,3];Zhang, Li[1]

机构：[1]GuangDong Ocean Univ, Agr Coll, Rd Haida 1, Zhanjiang 524088, Peoples R China;[2]South China Agr Univ, Guangdong Prov Key Lab Agroanim Genom & Mol Breed, Minist Agr, Guangzhou, Guangdong, Peoples R China;[3]South China Agr Univ, Key Lab Chicken Genet Breeding & Reprod, Minist Agr, Guangzhou, Guangdong, Peoples R China

年份：2019

卷号：682

起止页码：101

外文期刊名：GENE

收录：SCI-EXPANDED(收录号：WOS:000449899700010)、、WOS

基金：This work was supported by the Natural Science Foundation of China (31672412), the Natural Science Foundation of Guangdong Province (2017A030307002) and the Open Project of Key Lab of Chicken Genetics, Breeding and Reproduction, Ministry of Agriculture, China.

语种：英文

外文关键词：Growth hormone receptor; Natural antisense transcript; Stability; Double strand RNA

外文摘要：An increasing number of evidences indicated that long noncoding RNAs (LncRNAs) regulate a variety of biological progresses via different mechanisms. Our previous study had identified a chicken growth hormone receptor (GHR) antisense transcript (GHR-AS) which regulated GHR sense transcript (GHR-S) in LMH cells. In the present study, roles of GHR-AS and its regulatory mechanism were analyzed in chicken hepatocytes. The expression patterns of liver GHR-S, GHR-AS and Let-7b ascended with the development of chicken. The hepatocytes proliferation was promoted and more cells entered into DNA synthesis (S) phase when GHR-AS was over expressed while the cell proliferation was slowed and fewer cells were in S phase when GHR-AS was interfered. Meanwhile, the GHR-S increased when we overexpressed GHR-AS while it reduced when GHR-AS was inhibited. The S1 Nuclease protection assay indicated that GHR-S and GHR-AS formed RNA duplex via GHR-S 3' untranslation regon (3'UTR). In hepatocytes or LMH cells, the half-time of GHR-S showed a delayed trend when GHR-AS or GHR-AS 5' untranslation regon (5'UTR) was overexpressed. Furthermore, the level of GHR-S can be decreased by Let-7b mimics whereas it was partially rescued when co-transfected pGHR-AS or pGHR-AS 5'UTR with Let-7b mimics. Based on our findings, GHR-AS affected hepatocytes proliferation and improved GHR-S stability possibly by forming RNA duplex between GHR-S and GHR-AS, competing with Let-7b.