| 徐超亮,陈 磊,李 登,陈飞腾,徐子杰,邵 怡,沙明磊.LINC00472参与TGF-β1诱导的HK-2细胞系纤维化和上皮间充质转化[J].现代生物医学进展英文版,2021,(11):2007-2011. |
| LINC00472参与TGF-β1诱导的HK-2细胞系纤维化和上皮间充质转化 |
| LINC00472 is Involved in TGF-β1-induced Renal Fibrosis and Epithelial-mesenchymal Transition in HK-2 Cells |
| Received:November 23, 2020 Revised:December 18, 2020 |
| DOI：10.13241/j.cnki.pmb.2021.11.002 |
| 中文关键词: 肾纤维化 上皮间充质转化 慢性肾脏病 长链非编码RNA |
| 英文关键词: Renal fibrosis Epithelial-mesenchymal transition Chronic kidney disease Long non-coding RNAs |
| 基金项目:上海市浦江人才计划项目（2020PJD046）；上海市卫生健康委员会科研项目（202040071） |
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| 中文摘要: |
| 摘要 目的：探讨长链非编码RNA LINC00472在肾纤维化细胞模型中的表达及其在TGF-β1诱导的肾小管上皮细胞纤维化和上皮间充质转化（EMT）中的功能作用。方法：使用重组人TGF-β1诱导人肾小管上皮细胞（HK-2）纤维化和EMT，采用实时荧光定量PCR法检测细胞中纤维化相关基因和LINC00472的mRNA表达水平，通过Western blot免疫印迹法检测细胞中纤维化相关基因的蛋白表达水平，通过划痕实验评估LINC00472表达对HK-2细胞迁移能力的影响。结果：TGF-β1能成功诱导HK-2细胞发生纤维化和EMT，并剂量和时间依赖性地抑制LINC00472的表达（P<0.05）。抑制LINC00472进一步促进TGF-β1诱导的Fibronectin和Vimentin上调，以及E-cadherin下调（P<0.05）；而过表达LINC00472则能逆转TGF-β1对纤维化相关基因的诱导作用（P<0.05）。此外，抑制LINC00472能进一步增强TGF-β1诱导的HK-2细胞迁移（P<0.05），而上调LINC00472则使细胞迁移受到抑制（P<0.05）。结论：LINC00472在TGF-β1诱导的肾纤维化细胞模型中呈低表达，其表达水平的降低能促进细胞纤维化和EMT过程。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the expression of long non-coding RNA LINC00472 in an in vitro model of renal fibrosis and functional roles in renal fibrosis and tubular epithelial-mesenchymal transition (EMT). Methods: Recombinant human TGF-β1 were used to induce fibrosis and EMT of human renal tubular epithelial cells (HK-2). The mRNA expression levels of fibrosis-related genes and LINC00472 were measured by quantitative real-time PCR analysis, and the protein expression levels of fibrosis-related genes were detected by Western blot analysis. Wound healing assay was carried out to evaluate the impact of LINC00472 expression on HK-2 cells migration. Results: TGF-β1 successfully induced fibrosis and EMT of HK-2 cells, and inhibited LINC00472 expression in a dose- and time-dependent manner (P<0.05). LINC00472 knockdown further enhanced TGF-β1-induced upregulation of Fibronectin and Vimentin, and downregulation of E-cadherin (P<0.05), whereas LINC00472 overexpression significantly reversed the induction of fibrosis-related genes by TGF-β1 (P<0.05). Furthermore, LINC00472 inhibition further promoted TGF-β1-induced cell migration (P<0.05), while LINC00472 upregulation hindered cell migration (P<0.05). Conclusion: LINC00472 is low-expressed in TGF-β1-induced in vitro model of renal fibrosis, and its downregulation aggravates fibrosis and EMT of renal tubular cells. |
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