Evidence map›Paper›PMID 35190998›Full record

ArticleGenes & genomics2022

MicroRNA-183 accelerates the proliferation of hepatocyte during liver regeneration through targeting programmed cell death protein 6.

Fangxing Hou, Xing Li, Yanfeng Wang, Xiangzuo Xiao

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Article in Genes & genomics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.1field-weighted citation impact, top 64% of its field
1 · What the graph read from it

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3 · Its place in the literature

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0 citing papers in PubMed, 1 citations in OpenAlex.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Fangxing Hou *Queen Mary School, Nanchang University, Nanchang, Jiangxi, China.
Xing Li *Oncology Chemotherapy Department, Affiliated Haikou Hospital of Xiangya Medical College, Central South University, Haikou, Hainan, China.
Yanfeng WangDepartment of Pathology, Beidahuang Industry Group General Hospital, No. 235, hashuang Road, Nangang District, Harbin, 150000, China. wangyf_yanfeng@163.com.
Xiangzuo XiaoDepartment of Radiology, The First Affiliated Hospital of Nanchang University, No. 17 Yongwaizheng Street, Nanchang, 330006, Jiangxi, China. xiaoxxzuo_xia@163.com.
Nanchang University · CNCentral South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLiver 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.

objectiveThis study was aimed to explore the mechanism of miR-183 in on liver regeneration.

methodsAfter 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.

resultsMiR-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.

conclusionsCollectively, miR-183 promoted liver regeneration via targeting PDCD6.

Indexed as

Liver RegenerationAnimalsApoptosis Regulatory ProteinsBody WeightCalcium-Binding ProteinsCell ProliferationHepatocytesHumansMicroRNAsRatsApoptosis Regulatory ProteinsCalcium-Binding ProteinsMicroRNAsMIRN183 microRNA, humanMIRN183 microRNA, ratPDCD6 protein, humanHepatic indexHepatocytesLiver regenerationmicroRNA-183Partial hepatectomy

Identifiers

PMID35190998
OpenAlexW4213098952

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.