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Title: MiR-181b targets Six2 and inhibits the proliferation of metanephric mesenchymal cells in vitro

Abstract

Highlights: •We do bio-informatics websites to analysis of Six2 3′UTR. •MiR181b is a putative miRNA which can targets Six2 3′UTR. •MiR-181b binding site in the 3′UTR of Six2 is functional. •MiR-181b suppresses MK3 cells cell proliferation by targeting Six2. -- Abstract: MicroRNAs (miRNAs) are small non-coding RNAs that down-regulate gene expression by binding to target mRNA for cleavage or translational repression, and play important regulatory roles in renal development. Despite increasing genes have been predicted to be miRNA targets by bioinformatic analysis during kidney development, few of them have been verified by experiment. The objective of our study is to identify the miRNAs targeting Six2, a critical transcription factor that maintains the mesenchymal progenitor pool via self-renewal (proliferation) during renal development. We initially analyzed the 3′UTR of Six2 and found 37 binding sites targeted by 50 putative miRNAs in the 3′UTR of Six2. Among the 50 miRNAs, miR-181b is the miRNAs predicted by the three used websites. In our study, the results of luciferase reporter assay, realtime-PCR and Western blot demonstrated that miR-181b directly targeted on the 3′UTR of Six2 and down-regulate the expression of Six2 at mRNA and protein levels. Furthermore, EdU proliferation assay along with the Six2 rescuemore » strategy showed that miR-181b suppresses the proliferation of metanephric mesenchymal by targeting Six2 in part. In our research, we concluded that by targeting the transcription factor gene Six2, miR-181b inhibits the proliferation of metanephric mesenchymal cells in vitro and might play an important role in the formation of nephrons.« less

Authors:
; ; ; ;  [1];  [2]; ; ; ; ; ;  [1];  [1]
  1. The Division of Molecular Nephrology and the Creative Training Center for Undergraduates, The M.O.E. Key Laboratory of Laboratory Medical Diagnostics, The College of Laboratory Medicine, Chongqing Medical University, Chongqing 400016 (China)
  2. The Undergraduates Class of 2011 entry, The College of Laboratory Medicine, Chongqing Medical University, Chongqing 400016 (China)
Publication Date:
OSTI Identifier:
22242156
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 440; Journal Issue: 4; Other Information: Copyright (c) 2013 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; GENES; IN VITRO; KIDNEYS; LUCIFERASE; MESSENGER-RNA; POLYMERASE CHAIN REACTION; TRANSCRIPTION FACTORS

Citation Formats

Lyu, Zhongshi, Mao, Zhaomin, Wang, Honglian, Fang, Yin, Chen, Tielin, Wan, Qianya, Wang, Ming, Wang, Nian, Xiao, Jiangming, Wei, Hongyuan, Li, Xun, Liu, Yi, and Zhou, Qin. MiR-181b targets Six2 and inhibits the proliferation of metanephric mesenchymal cells in vitro. United States: N. p., 2013. Web. doi:10.1016/J.BBRC.2013.09.059.
Lyu, Zhongshi, Mao, Zhaomin, Wang, Honglian, Fang, Yin, Chen, Tielin, Wan, Qianya, Wang, Ming, Wang, Nian, Xiao, Jiangming, Wei, Hongyuan, Li, Xun, Liu, Yi, & Zhou, Qin. MiR-181b targets Six2 and inhibits the proliferation of metanephric mesenchymal cells in vitro. United States. https://doi.org/10.1016/J.BBRC.2013.09.059
Lyu, Zhongshi, Mao, Zhaomin, Wang, Honglian, Fang, Yin, Chen, Tielin, Wan, Qianya, Wang, Ming, Wang, Nian, Xiao, Jiangming, Wei, Hongyuan, Li, Xun, Liu, Yi, and Zhou, Qin. 2013. "MiR-181b targets Six2 and inhibits the proliferation of metanephric mesenchymal cells in vitro". United States. https://doi.org/10.1016/J.BBRC.2013.09.059.
@article{osti_22242156,
title = {MiR-181b targets Six2 and inhibits the proliferation of metanephric mesenchymal cells in vitro},
author = {Lyu, Zhongshi and Mao, Zhaomin and Wang, Honglian and Fang, Yin and Chen, Tielin and Wan, Qianya and Wang, Ming and Wang, Nian and Xiao, Jiangming and Wei, Hongyuan and Li, Xun and Liu, Yi and Zhou, Qin},
abstractNote = {Highlights: •We do bio-informatics websites to analysis of Six2 3′UTR. •MiR181b is a putative miRNA which can targets Six2 3′UTR. •MiR-181b binding site in the 3′UTR of Six2 is functional. •MiR-181b suppresses MK3 cells cell proliferation by targeting Six2. -- Abstract: MicroRNAs (miRNAs) are small non-coding RNAs that down-regulate gene expression by binding to target mRNA for cleavage or translational repression, and play important regulatory roles in renal development. Despite increasing genes have been predicted to be miRNA targets by bioinformatic analysis during kidney development, few of them have been verified by experiment. The objective of our study is to identify the miRNAs targeting Six2, a critical transcription factor that maintains the mesenchymal progenitor pool via self-renewal (proliferation) during renal development. We initially analyzed the 3′UTR of Six2 and found 37 binding sites targeted by 50 putative miRNAs in the 3′UTR of Six2. Among the 50 miRNAs, miR-181b is the miRNAs predicted by the three used websites. In our study, the results of luciferase reporter assay, realtime-PCR and Western blot demonstrated that miR-181b directly targeted on the 3′UTR of Six2 and down-regulate the expression of Six2 at mRNA and protein levels. Furthermore, EdU proliferation assay along with the Six2 rescue strategy showed that miR-181b suppresses the proliferation of metanephric mesenchymal by targeting Six2 in part. In our research, we concluded that by targeting the transcription factor gene Six2, miR-181b inhibits the proliferation of metanephric mesenchymal cells in vitro and might play an important role in the formation of nephrons.},
doi = {10.1016/J.BBRC.2013.09.059},
url = {https://www.osti.gov/biblio/22242156}, journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 4,
volume = 440,
place = {United States},
year = {Fri Nov 01 00:00:00 EDT 2013},
month = {Fri Nov 01 00:00:00 EDT 2013}
}