Jie Zhao1, Ye Fan1, Kunpeng Wang1, Xuhao Ni1, Jian Gu1, Hao Lu1, Yunjie Lu1, Ling Lu1, Xinzheng Dai1, Xuehao Wang2. 1. Liver Transplantation Center of the First Affiliated Hospital and Key Laboratory on Living Donor Liver Transplantation, Ministry of Health, Nanjing Medical University, Nanjing, Jiangsu Province, PR China. 2. Liver Transplantation Center of the First Affiliated Hospital and Key Laboratory on Living Donor Liver Transplantation, Ministry of Health, Nanjing Medical University, Nanjing, Jiangsu Province, PR China. Electronic address: wangxuehao1941@hotmail.com.
Abstract
BACKGROUND AND AIMS: Recently, a couple of the long noncoding RNAs (lncRNAs) have been proved to participate in hepatocellular carcinoma development and progression. However, their associations with liver cirrhosis have not been reported. In this study, we aimed to identify the affection of HULC on regulatory T cells (Tregs) differentiation in HBV-related liver cirrhosis. METHODS: Seven lncRNAs were chosen as candidate lncRNAs based on the association with liver disease. The candidate lncRNAs were validated by RT-qPCR. Additional flow cytometry of Tregs was performed in 34 HBV-related liver cirrhosis patients and 34 healthy volunteers. To investigate the function of HULC, HULC expression was modified by gene overexpression via lentivirus vector. RIP assay was performed further to validate the association between HULC and p18. RESULTS: Circulation Tregs and HULC were significantly up-regulated in plasma samples of HBV-related cirrhosis patients. In addition, overexpression of HULC by lentivirus vector elevated Treg frequency in vitro. Furthermore, RIP assay showed that HULC down-regulated the level of p18 directly. CONCLUSIONS: We confirmed the effects of HULC on Tregs differentiation in HBV-related liver cirrhosis. In addition, it was proved that HULC regulates the function of Tregs through down-regulated the level of p18 directly.
BACKGROUND AND AIMS: Recently, a couple of the long noncoding RNAs (lncRNAs) have been proved to participate in hepatocellular carcinoma development and progression. However, their associations with liver cirrhosis have not been reported. In this study, we aimed to identify the affection of HULC on regulatory T cells (Tregs) differentiation in HBV-related liver cirrhosis. METHODS: Seven lncRNAs were chosen as candidate lncRNAs based on the association with liver disease. The candidate lncRNAs were validated by RT-qPCR. Additional flow cytometry of Tregs was performed in 34 HBV-related liver cirrhosispatients and 34 healthy volunteers. To investigate the function of HULC, HULC expression was modified by gene overexpression via lentivirus vector. RIP assay was performed further to validate the association between HULC and p18. RESULTS: Circulation Tregs and HULC were significantly up-regulated in plasma samples of HBV-related cirrhosispatients. In addition, overexpression of HULC by lentivirus vector elevated Treg frequency in vitro. Furthermore, RIP assay showed that HULC down-regulated the level of p18 directly. CONCLUSIONS: We confirmed the effects of HULC on Tregs differentiation in HBV-related liver cirrhosis. In addition, it was proved that HULC regulates the function of Tregs through down-regulated the level of p18 directly.