LncRNA CRNDE通过靶向miR-29a-3p调节肾上皮细胞-间充质-上皮转化参与肾纤维化的发病机制

IF 1.5 4区医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis Pub Date : 2023-01-01 DOI:10.1016/j.mrfmmm.2023.111817

Min Zhao, Nan Li, Cheng Wan, Qingyan Zhang, Hengjin Wang, Chunming Jiang

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引用次数: 0

摘要

先前的研究结果表明，肾纤维化和上皮-间质转化（EMT）在肾纤维化过程中发挥着重要作用，但其潜在机制尚不清楚。长编码RNA（lncRNA）CRNDE已成为EMT程序的有效调节因子，因此，在本工作中，我们研究了lncRNA CRNDE/miR-29a-3p轴在肾纤维化中的作用及其潜在机制。我们发现，在肾纤维化动物和细胞模型中，通过TGF-β的治疗，lncRNA CRNDE在动物模型或细胞中动态上调。此外，CRNDE对大鼠的敲除可显著抑制EMT，防止肾纤维化。最后，CRNDE通过抑制miR-29a-3p的表达来调节肾纤维化。总之，我们的研究结果表明，CRNDE通过靶向miR-29a-3p作为肾纤维化的调节因子。我们的发现可能为治疗肾纤维化提供一个潜在的治疗靶点。

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LncRNA CRNDE is involved in the pathogenesis of renal fibrosis by regulating renal epithelial cell mesenchymal-epithelial transition via targeting miR-29a-3p

Results of previous studies suggested that renal fibrosis and epithelial-mesenchymal transition (EMT) plays an important role in the process of renal fibrosis, but the underlying mechanism remains unclear. Long coding RNA (lncRNA) CRNDE has emerged as potent regulators of EMT programs, therefore, in present work, we examined the roles of LncRNA CRNDE/miR-29a-3p axis in renal fibrosis and the underlying mechanism. We found that in both renal fibrosis animal and cell models, lncRNA CRNDE was dynamically upregulated in animal models or cells by the treatment of TGF-β. Furthermore, knockdown of CRNDE to rat significantly inhibited EMT, prevented renal fibrosis. Finally, CRNDE regulates renal fibrosis through suppression of miR-29a-3p expression. Together, our results demonstrated that CRNDE acted as a regulator of renal fibrosis via targeting miR-29a-3p. Our findings may provide a potential therapeutic target for the treatment of renal fibrosis.

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来源期刊

Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis 生物-毒理学

CiteScore

4.90

自引率

0.00%

发文量

审稿时长

51 days

期刊介绍： Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs. MR publishes articles in the following areas: Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence. The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance. Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing. Landscape of somatic mutations and epimutations in cancer and aging. Role of de novo mutations in human disease and aging; mutations in population genomics. Interactions between mutations and epimutations. The role of epimutations in chromatin structure and function. Mitochondrial DNA mutations and their consequences in terms of human disease and aging. Novel ways to generate mutations and epimutations in cell lines and animal models.