MiR-92a-3p Knockdown Attenuates Transforming Growth Factor-β1-induced Tubulointerstitial Fibrosis by Targeting LIN28A-mediated EMT Pathway

The role of microRNAs in regulating tubulointerstitial fibrosis, a key feature of progressive chronic kidney disease, is of significant importance. LIN28A has been reported to attenuate renal fibrosis in obstructive nephropathy. Here, our objective was to investigate the precise biological function...

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Main Authors: Mingzhi Xu, Mingjiao Pang, Chunli Wang, Na An, Ruman Chen, Yafei Bai, Jiqing He, Yonghui Qi#
Format: Article
Language:English
Published: Wolters Kluwer Medknow Publications 2024-08-01
Series:Journal of Physiological Investigation
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Online Access:https://journals.lww.com/10.4103/ejpi.EJPI-D-24-00019
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author Mingzhi Xu
Mingjiao Pang
Chunli Wang
Na An
Ruman Chen
Yafei Bai
Jiqing He
Chunli Wang
Yonghui Qi#
author_facet Mingzhi Xu
Mingjiao Pang
Chunli Wang
Na An
Ruman Chen
Yafei Bai
Jiqing He
Chunli Wang
Yonghui Qi#
author_sort Mingzhi Xu
collection DOAJ
description The role of microRNAs in regulating tubulointerstitial fibrosis, a key feature of progressive chronic kidney disease, is of significant importance. LIN28A has been reported to attenuate renal fibrosis in obstructive nephropathy. Here, our objective was to investigate the precise biological function of the miR-92a-3p/LIN28A axis in tubulointerstitial fibrosis. The human renal proximal tubular epithelial (HK-2) cell line was exposed to transforming growth factor (TGF)-β1, establishing an in vitro model mimicking tubulointerstitial fibrosis. Luciferase reporter assay was utilized to investigate the relationship between miR-92a-3p and LIN28A. Cell transfection techniques were employed to modify the expression of miR-92a-3p and LIN28A. An in vivo model of tubulointerstitial fibrosis was created by inducing unilateral ureteral obstruction (UUO) in C57BL/6N mice. Our initial observations showed that TGF-β1 treatment of HK-2 cells and the UUO mice model led to an increase in miR-92a-3p expression and a decrease in LIN28A expression. We confirmed that miR-92a-3p directly targeted LIN28A in HK-2 cells. In TGF-β1-stimulated HK-2 cells, knocking down miR-92a-3p notably reduced the levels of alpha smooth muscle actin and vimentin and concurrently enhanced the expression of E-cadherin. These changes were counteracted upon transfection with si-LIN28A. Thus, directing interventions toward miR-92a-3p holds the potential to emerge as a viable therapeutic approach for addressing tubulointerstitial fibrosis.
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spelling doaj-art-1c10cdc30bcd40659cd88a243598e23d2025-08-20T02:09:47ZengWolters Kluwer Medknow PublicationsJournal of Physiological Investigation2950-63442950-63522024-08-0167419820610.4103/ejpi.EJPI-D-24-00019MiR-92a-3p Knockdown Attenuates Transforming Growth Factor-β1-induced Tubulointerstitial Fibrosis by Targeting LIN28A-mediated EMT PathwayMingzhi XuMingjiao PangChunli WangNa AnRuman ChenYafei BaiJiqing HeChunli WangYonghui Qi#The role of microRNAs in regulating tubulointerstitial fibrosis, a key feature of progressive chronic kidney disease, is of significant importance. LIN28A has been reported to attenuate renal fibrosis in obstructive nephropathy. Here, our objective was to investigate the precise biological function of the miR-92a-3p/LIN28A axis in tubulointerstitial fibrosis. The human renal proximal tubular epithelial (HK-2) cell line was exposed to transforming growth factor (TGF)-β1, establishing an in vitro model mimicking tubulointerstitial fibrosis. Luciferase reporter assay was utilized to investigate the relationship between miR-92a-3p and LIN28A. Cell transfection techniques were employed to modify the expression of miR-92a-3p and LIN28A. An in vivo model of tubulointerstitial fibrosis was created by inducing unilateral ureteral obstruction (UUO) in C57BL/6N mice. Our initial observations showed that TGF-β1 treatment of HK-2 cells and the UUO mice model led to an increase in miR-92a-3p expression and a decrease in LIN28A expression. We confirmed that miR-92a-3p directly targeted LIN28A in HK-2 cells. In TGF-β1-stimulated HK-2 cells, knocking down miR-92a-3p notably reduced the levels of alpha smooth muscle actin and vimentin and concurrently enhanced the expression of E-cadherin. These changes were counteracted upon transfection with si-LIN28A. Thus, directing interventions toward miR-92a-3p holds the potential to emerge as a viable therapeutic approach for addressing tubulointerstitial fibrosis.https://journals.lww.com/10.4103/ejpi.EJPI-D-24-00019chronic kidney diseaselin28amir-92a-3ptubulointerstitial fibrosis
spellingShingle Mingzhi Xu
Mingjiao Pang
Chunli Wang
Na An
Ruman Chen
Yafei Bai
Jiqing He
Chunli Wang
Yonghui Qi#
MiR-92a-3p Knockdown Attenuates Transforming Growth Factor-β1-induced Tubulointerstitial Fibrosis by Targeting LIN28A-mediated EMT Pathway
Journal of Physiological Investigation
chronic kidney disease
lin28a
mir-92a-3p
tubulointerstitial fibrosis
title MiR-92a-3p Knockdown Attenuates Transforming Growth Factor-β1-induced Tubulointerstitial Fibrosis by Targeting LIN28A-mediated EMT Pathway
title_full MiR-92a-3p Knockdown Attenuates Transforming Growth Factor-β1-induced Tubulointerstitial Fibrosis by Targeting LIN28A-mediated EMT Pathway
title_fullStr MiR-92a-3p Knockdown Attenuates Transforming Growth Factor-β1-induced Tubulointerstitial Fibrosis by Targeting LIN28A-mediated EMT Pathway
title_full_unstemmed MiR-92a-3p Knockdown Attenuates Transforming Growth Factor-β1-induced Tubulointerstitial Fibrosis by Targeting LIN28A-mediated EMT Pathway
title_short MiR-92a-3p Knockdown Attenuates Transforming Growth Factor-β1-induced Tubulointerstitial Fibrosis by Targeting LIN28A-mediated EMT Pathway
title_sort mir 92a 3p knockdown attenuates transforming growth factor β1 induced tubulointerstitial fibrosis by targeting lin28a mediated emt pathway
topic chronic kidney disease
lin28a
mir-92a-3p
tubulointerstitial fibrosis
url https://journals.lww.com/10.4103/ejpi.EJPI-D-24-00019
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