lncRNA TUG1 regulates hyperuricemia-induced renal <?A3B2 pi6?>fibrosis in a rat model

Renal fibrosis is most common among chronic kidney diseases. Molecular studies have shown that long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) participate in renal fibrosis, while the roles of lncRNA taurine upregulated gene 1 (TUG1) and miR-140-3p in hyperuricemia-induced renal fibrosis remain...

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Main Authors: Zhang Ying, Zhang Haizhen, Hu Langtao, Wei Jiali, Ma Chunyang
Format: Article
Language:English
Published: China Science Publishing & Media Ltd. 2022-09-01
Series:Acta Biochimica et Biophysica Sinica
Subjects:
Online Access:https://www.sciengine.com/doi/10.3724/abbs.2022128
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author Zhang Ying
Zhang Haizhen
Hu Langtao
Wei Jiali
Ma Chunyang
author_facet Zhang Ying
Zhang Haizhen
Hu Langtao
Wei Jiali
Ma Chunyang
author_sort Zhang Ying
collection DOAJ
description Renal fibrosis is most common among chronic kidney diseases. Molecular studies have shown that long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) participate in renal fibrosis, while the roles of lncRNA taurine upregulated gene 1 (TUG1) and miR-140-3p in hyperuricemia-induced renal fibrosis remain less investigated. In this study, a rat hyperuricemia model is constructed by oral administration of adenine. TUG1, miR-140-3p, and cathepsin D (CtsD) expression levels in rat models are measured. After altering TUG1, miR-140-3p, or CtsD expression in modelled rats, biochemical indices, including uric acid (UA), serum creatine (SCr), blood urea nitrogen (BUN), and 24-h urine protein are detected, pathological changes in the renal tissues, and renal fibrosis are examined. In renal tissues from hyperuricemic rats, TUG1 and CtsD are upregulated, while miR-140-3p is downregulated. Inhibiting TUG1 or CtsD or upregulating miR-140-3p relieves renal fibrosis in hyperuricemic rats. Downregulated miR-140-3p reverses the therapeutic effect of TUG1 reduction, while overexpression of CtsD abolishes the role of miR-140-3p upregulation in renal fibrosis. Collectively, this study highlights that TUG1 inhibition upregulates miR-140-3p to ameliorate renal fibrosis in hyperuricemic rats by inhibiting CtsD.
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spelling doaj.art-aedb42c9fcda497db3c6f785725042942023-11-07T01:01:41ZengChina Science Publishing & Media Ltd.Acta Biochimica et Biophysica Sinica1672-91452022-09-01541365137510.3724/abbs.202212820d259cclncRNA TUG1 regulates hyperuricemia-induced renal <?A3B2 pi6?>fibrosis in a rat modelZhang Ying0Zhang Haizhen1Hu Langtao2Wei Jiali3Ma Chunyang4["Department of Nephrology, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China"]["Department of Nephrology, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China"]["Department of Nephrology, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China"]["Department of Nephrology, Hainan General Hospital (Hainan Affiliated Hospital of Hainan Medical University), Haikou 570311, China"]["of Neurosurgery, First Affiliated Hospital of Hainan Medical University, Haikou 570100, China"]Renal fibrosis is most common among chronic kidney diseases. Molecular studies have shown that long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) participate in renal fibrosis, while the roles of lncRNA taurine upregulated gene 1 (TUG1) and miR-140-3p in hyperuricemia-induced renal fibrosis remain less investigated. In this study, a rat hyperuricemia model is constructed by oral administration of adenine. TUG1, miR-140-3p, and cathepsin D (CtsD) expression levels in rat models are measured. After altering TUG1, miR-140-3p, or CtsD expression in modelled rats, biochemical indices, including uric acid (UA), serum creatine (SCr), blood urea nitrogen (BUN), and 24-h urine protein are detected, pathological changes in the renal tissues, and renal fibrosis are examined. In renal tissues from hyperuricemic rats, TUG1 and CtsD are upregulated, while miR-140-3p is downregulated. Inhibiting TUG1 or CtsD or upregulating miR-140-3p relieves renal fibrosis in hyperuricemic rats. Downregulated miR-140-3p reverses the therapeutic effect of TUG1 reduction, while overexpression of CtsD abolishes the role of miR-140-3p upregulation in renal fibrosis. Collectively, this study highlights that TUG1 inhibition upregulates miR-140-3p to ameliorate renal fibrosis in hyperuricemic rats by inhibiting CtsD.https://www.sciengine.com/doi/10.3724/abbs.2022128hyperuricemiarenal fibrosistaurine upregulated gene 1miR-140-3pcathepsin D
spellingShingle Zhang Ying
Zhang Haizhen
Hu Langtao
Wei Jiali
Ma Chunyang
lncRNA TUG1 regulates hyperuricemia-induced renal <?A3B2 pi6?>fibrosis in a rat model
Acta Biochimica et Biophysica Sinica
hyperuricemia
renal fibrosis
taurine upregulated gene 1
miR-140-3p
cathepsin D
title lncRNA TUG1 regulates hyperuricemia-induced renal <?A3B2 pi6?>fibrosis in a rat model
title_full lncRNA TUG1 regulates hyperuricemia-induced renal <?A3B2 pi6?>fibrosis in a rat model
title_fullStr lncRNA TUG1 regulates hyperuricemia-induced renal <?A3B2 pi6?>fibrosis in a rat model
title_full_unstemmed lncRNA TUG1 regulates hyperuricemia-induced renal <?A3B2 pi6?>fibrosis in a rat model
title_short lncRNA TUG1 regulates hyperuricemia-induced renal <?A3B2 pi6?>fibrosis in a rat model
title_sort lncrna tug1 regulates hyperuricemia induced renal a3b2 pi6 fibrosis in a rat model
topic hyperuricemia
renal fibrosis
taurine upregulated gene 1
miR-140-3p
cathepsin D
url https://www.sciengine.com/doi/10.3724/abbs.2022128
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AT hulangtao lncrnatug1regulateshyperuricemiainducedrenala3b2pi6fibrosisinaratmodel
AT weijiali lncrnatug1regulateshyperuricemiainducedrenala3b2pi6fibrosisinaratmodel
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