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miR-328 prevents renal fibrogenesis by directly targeting TGF-β2

W He, J Zhuang, Z G Zhao

    Bratislavske Lekarske Listy
    |August 31, 2018
    PubMed

    Insights

    MicroRNA-328 (miR-328) prevents kidney fibrosis by targeting TGF-β2. Upregulating miR-328 may offer a new therapeutic strategy for treating renal fibrosis.

    Area of Science:

    • Molecular Biology
    • Cell Biology
    • Nephrology

    Background:

    • MicroRNAs regulate gene expression post-transcriptionally.
    • Aberrant microRNA expression is linked to human diseases, including renal fibrosis.
    • The specific role of miR-328 in renal fibrogenesis remains largely unknown.

    Purpose of the Study:

    • To investigate the expression profile of miR-328 in a cell model of renal fibrosis.
    • To elucidate the regulatory mechanisms of miR-328 in renal fibrogenesis.
    • To determine if miR-328 can be a therapeutic target for renal fibrosis.

    Main Methods:

    • Quantitative reverse transcription PCR (qRT-PCR) to assess miR-328 expression.
    • Bioinformatical analysis to identify potential miR-328 target genes.
    • Luciferase reporter assay to confirm direct targeting.
    • Transfection with miR-328 mimics to study its functional effects.

    Main Results:

    • Transforming growth factor-beta 1 (TGF-β1) induced epithelial-mesenchymal transition (EMT) and fibrogenesis, while down-regulating miR-328.
    • TGF-β2 was identified as a direct target gene of miR-328.
    • Upregulation of miR-328 significantly repressed TGF-β2 and extracellular matrix (ECM) protein expression.
    • miR-328 mimics successfully increased miR-328 expression.

    Conclusions:

    • miR-328 directly targets TGF-β2, thereby preventing renal fibrogenesis.
    • Elevated miR-328 levels demonstrate potential as a novel therapeutic strategy for renal fibrosis.
    Keywords:
    ECM EMT.TGF-βmiR-328miRNArenal fibrosis

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