Fangxing Hou1, Xing Li2, Yanfeng Wang3, Xiangzuo Xiao4. 1. Queen Mary School, Nanchang University, Nanchang, Jiangxi, China. 2. Oncology Chemotherapy Department, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, China. 3. Department of Pathology, Beidahuang Industry Group General Hospital, No. 235, hashuang Road, Nangang District, Harbin, 150000, China. wangyf_yanfeng@163.com. 4. Department of Radiology, The First Affiliated Hospital of Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330006, Jiangxi, China. xiaoxxzuo_xia@163.com.
Abstract
BACKGROUND: Liver regeneration is a highly orchestrated process concerning the modulation of various microRNAs (miRs). miR-183 was recently found to be involved in the process of liver regeneration, that miR-183 was remarkably up-regulated at 2-6 h after partial hepatectomy. OBJECTIVE: This study was aimed to explore the mechanism of miR-183 in on liver regeneration. METHODS: After partial hepatectomy (PH) or transfection, we measured the changes of miR-183 and programmed cell death protein 6 (PDCD6) levels in rats and the hepatocytes. The histopathology was observed with hematoxylin-eosin staining. The miR-183 mimic and inhibitor plasmids were intravenously injected into rats, and the liver weight/body weight ratio was calculated. The prediction of TargetScan and the validation of luciferase activity assay were employed to confirm the targeting relationship between miR-183 and PDCD6. The viability, apoptosis and cell cycle of transfected rat hepatocyte BRL-3A were determined via MTT and flow cytometry assays. RESULTS: MiR-183 expression showed a contrary tendency with that of PDCD6 during liver regeneration. Enhanced miR-183 in rats could notably increase liver/body weight ratio, while its inhibition did conversely. Overexpressed PDCD6, a target of miR-183, repressed the viability and cell cycle in hepatocytes, whereas its silence led to contrary results. Overexpressed miR-183 in BRL-3A cells enhanced cell viability and promoted the cell cycle yet suppressed apoptosis, whereas its inhibition showed contrary results, which were offset by PDCD6. CONCLUSIONS: Collectively, miR-183 promoted liver regeneration via targeting PDCD6.
BACKGROUND: Liver regeneration is a highly orchestrated process concerning the modulation of various microRNAs (miRs). miR-183 was recently found to be involved in the process of liver regeneration, that miR-183 was remarkably up-regulated at 2-6 h after partial hepatectomy. OBJECTIVE: This study was aimed to explore the mechanism of miR-183 in on liver regeneration. METHODS: After partial hepatectomy (PH) or transfection, we measured the changes of miR-183 and programmed cell death protein 6 (PDCD6) levels in rats and the hepatocytes. The histopathology was observed with hematoxylin-eosin staining. The miR-183 mimic and inhibitor plasmids were intravenously injected into rats, and the liver weight/body weight ratio was calculated. The prediction of TargetScan and the validation of luciferase activity assay were employed to confirm the targeting relationship between miR-183 and PDCD6. The viability, apoptosis and cell cycle of transfected rat hepatocyte BRL-3A were determined via MTT and flow cytometry assays. RESULTS: MiR-183 expression showed a contrary tendency with that of PDCD6 during liver regeneration. Enhanced miR-183 in rats could notably increase liver/body weight ratio, while its inhibition did conversely. Overexpressed PDCD6, a target of miR-183, repressed the viability and cell cycle in hepatocytes, whereas its silence led to contrary results. Overexpressed miR-183 in BRL-3A cells enhanced cell viability and promoted the cell cycle yet suppressed apoptosis, whereas its inhibition showed contrary results, which were offset by PDCD6. CONCLUSIONS: Collectively, miR-183 promoted liver regeneration via targeting PDCD6.
Authors: B Björnsson; E Sparrelid; B Røsok; E Pomianowska; K Hasselgren; T Gasslander; B A Bjørnbeth; B Isaksson; P Sandström Journal: Eur J Surg Oncol Date: 2016-01-21 Impact factor: 4.424