Related Experiment Video
Updated: Mar 29, 2026

Induction and Analysis of Epithelial to Mesenchymal Transition
Published on: August 27, 2013
MiR542-3p Regulates the Epithelial-Mesenchymal Transition by Directly Targeting BMP7 in NRK52e
Zhicheng Liu1, Yuru Zhou2, Yue Yuan3
1The 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. liuzhicheng323@163.com.
Abstract:
Accumulating evidence demonstrated that miRNAs are highly involved in kidney fibrosis and Epithelial-Eesenchymal Transition (EMT), however, the mechanisms of miRNAs in kidney fibrosis are poorly understood. In this work, we identified that miR542-3p could promote EMT through down-regulating bone morphogenetic protein 7 (BMP7) expression by targeting BMP7 3'UTR. Firstly, real-time PCR results showed that miR542-3p was significantly up-regulated in kidney fibrosis in vitro and in vivo. Moreover, Western blot results demonstrated that miR542-3p may promote EMT in the NRK52e cell line. In addition, we confirmed that BMP7, which played a crucial role in anti-kidney fibrosis and suppressed the progression of EMT, was a target of miR542-3p through Dual-Luciferase reporter assay, as did Western blot analysis. The effects of miR542-3p on regulating EMT could also be suppressed by transiently overexpressing BMP7 in NRK52e cells. Taken together, miR542-3p may be a critical mediator of the induction of EMT via directly targeting BMP7.
Insights
MicroRNAs regulate kidney fibrosis and Epithelial-Mesenchymal Transition (EMT). This study reveals miR542-3p promotes kidney fibrosis and EMT by down-regulating bone morphogenetic protein 7 (BMP7).
Area of Science:
- Molecular Biology
- Renal Physiology
- Biochemistry
Background:
- MicroRNAs (miRNAs) are implicated in kidney fibrosis and Epithelial-Mesenchymal Transition (EMT).
- The precise mechanisms by which miRNAs contribute to kidney fibrosis remain incompletely understood.
- Understanding these mechanisms is crucial for developing targeted therapies.
Purpose of the Study:
- To elucidate the role and mechanism of miR542-3p in kidney fibrosis and EMT.
- To identify the direct molecular targets of miR542-3p involved in these processes.
- To explore the therapeutic potential of targeting the miR542-3p/BMP7 axis.
Main Methods:
- Quantitative real-time PCR to assess miR542-3p expression in kidney fibrosis models.
- Western blot analysis to evaluate EMT markers and protein expression in NRK52e cells.
- Dual-Luciferase reporter assay to confirm the direct targeting of BMP7 by miR542-3p.
Main Results:
- miR542-3p was significantly upregulated in both in vitro and in vivo models of kidney fibrosis.
- miR542-3p was shown to promote EMT in NRK52e cells.
- Bone morphogenetic protein 7 (BMP7) was identified as a direct target of miR542-3p, with miR542-3p down-regulating BMP7 expression.
- Overexpression of BMP7 counteracted the EMT-promoting effects of miR542-3p.
Conclusions:
- miR542-3p acts as a key mediator in the induction of EMT during kidney fibrosis.
- The mechanism involves the direct targeting and down-regulation of BMP7 by miR542-3p.
- miR542-3p represents a potential therapeutic target for kidney fibrosis and EMT.
Related Concept Videos
MAPK Signaling Cascades
PI3K/mTOR/AKT Signaling Pathway
Metastasis
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
Master Transcription Regulators

