Journal
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
Volume 54, Issue 9, Pages 1365-1375Publisher
SCIENCE PRESS
DOI: 10.3724/abbs.2022128
Keywords
hyperuricemia; renal fibrosis; taurine upregulated gene 1; miR-140-3p; cathepsin D
Categories
Funding
- National Natural Science Foundation of China [82160135]
- Hainan Key Research and Development Project [ZDYF2022SHFZ016]
- Hainan Provincial Natural Science Foundation of China [822QN455, 821MS0825]
- Hainan Province Clinical Medical Research Center of NephrologyHainan Province Clinical Medical Center
- National Natural Science Fund Cultivating 530 Projects of Hainan General Hospital [2021MSXM17, 2021QNXM03, 2021QNXM06, 2021QNXM12, 2021QNXM13, 2021QNXM17]
- Projects of Hainan General Hospital [QN202008, QN202007]
Ask authors/readers for more resources
Renal fibrosis is a common complication of chronic kidney diseases. This study investigates the roles of lncRNA TUG1 and miR-140-3p in hyperuricemia-induced renal fibrosis. The results show that inhibiting TUG1 or CtsD or upregulating miR-140-3p can alleviate renal fibrosis in hyperuricemic rats. The study highlights the potential therapeutic effects of targeting TUG1, miR-140-3p, and CtsD in the treatment of renal fibrosis.
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available