Xiaoyan Li, Hongxia Peng, Qing Feng, Shumei Zhong, Yi Li, Yingling Zheng, Guang Yang
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Subsequently, The effect of OIP5-AS1 on TGF-β1-induced fibrosis in HK2 cells was investigated by assessing cell proliferation using the CCK-8 assay and analyzing the expression of fibrosis- and EMT-related proteins through WB.. The targeting relationship between OIP5-AS1 and miR-181a-5p, as well as the influence of OIP5-AS1 on miR-181a-5p expression, was investigated using a dual-luciferase reporter assay. Subsequently, the impact of miR-181a-5p upregulation on the proliferation of TGF-β1-induced HK2 cells was examined through a CCK-8 assay.</p><p><strong>Results: </strong>The study found that TGF-β1 treatment upregulated OIP5-AS1, α-SMA, Col-IV, and FN in HK2 cells while downregulating miR-181a-5p and E-cadherin. OIP5-AS1 downregulation promoted cell proliferation and inhibited fibrosis-related proteins. MiR-181a-5p was identified as a direct target of OIP5-AS1, and its upregulation enhanced cell proliferation. Conclusion . 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引用次数: 0
摘要
本研究旨在通过OIP5-AS1与miR-181a-5p的相互作用，探讨其在纤维化细胞模型中的作用。方法：采用TGF-β1诱导人肾小管上皮细胞（HK2），建立体外纤维化模型。采用定量实时聚合酶链式反应（qPCR）检测对照组（正常）和模型组（TGF-β1）中OIP5-AS1和miR-181a-5p的表达水平。采用qPCR和Western Blot （WB）检测两组细胞中与纤维化和EMT相关的基因和蛋白的表达情况。随后，通过CCK-8法评估细胞增殖，并通过WB分析纤维化相关蛋白和emt相关蛋白的表达，研究OIP5-AS1对TGF-β1诱导的HK2细胞纤维化的影响。采用双荧光素酶报告基因法研究了OIP5-AS1与miR-181a-5p的靶向关系，以及OIP5-AS1对miR-181a-5p表达的影响。随后，通过CCK-8实验检测miR-181a-5p上调对TGF-β1诱导的HK2细胞增殖的影响。结果：研究发现TGF-β1处理上调HK2细胞OIP5-AS1、α-SMA、Col-IV、FN，下调miR-181a-5p、E-cadherin。OIP5-AS1下调可促进细胞增殖，抑制纤维化相关蛋白。MiR-181a-5p被确定为OIP5-AS1的直接靶点，其上调可增强细胞增殖。结论。OIP5-AS1的抑制通过调控miR-181a-5p减弱TGF-β1诱导的HK2细胞纤维化。
The lncRNA OIP5-AS1/miR-181a-5p Axis Promotes TGF-β1-induced Fibrosis in HK2 Cells.
Introduction: Th is study was conducted to explore the role of OIP5-AS1 in a fibrosis cell model through its interaction with miR-181a-5p.
Methods: An in-vitro fibrosis model was established by inducing human renal tubular epithelial cells (HK2) with TGF-β1. The expression levels of OIP5-AS1 and miR-181a-5p in the control (Normal) and model (TGF-β1) groups were measured using Quantitative Real-time Polymerase Chain Reaction (qPCR).. qPCR and Western Blot (WB) were used to detect the expression of genes and proteins related to fibrosis and EMT in the two groups of cells. Subsequently, The effect of OIP5-AS1 on TGF-β1-induced fibrosis in HK2 cells was investigated by assessing cell proliferation using the CCK-8 assay and analyzing the expression of fibrosis- and EMT-related proteins through WB.. The targeting relationship between OIP5-AS1 and miR-181a-5p, as well as the influence of OIP5-AS1 on miR-181a-5p expression, was investigated using a dual-luciferase reporter assay. Subsequently, the impact of miR-181a-5p upregulation on the proliferation of TGF-β1-induced HK2 cells was examined through a CCK-8 assay.
Results: The study found that TGF-β1 treatment upregulated OIP5-AS1, α-SMA, Col-IV, and FN in HK2 cells while downregulating miR-181a-5p and E-cadherin. OIP5-AS1 downregulation promoted cell proliferation and inhibited fibrosis-related proteins. MiR-181a-5p was identified as a direct target of OIP5-AS1, and its upregulation enhanced cell proliferation. Conclusion . The suppression of OIP5-AS1 attenuates TGF-β1-induced fibrosis in HK2 cells through the regulation of miR-181a-5p.
期刊介绍：
The Iranian Journal of Kidney Diseases (IJKD), a peer-reviewed journal in English, is the official publication of the Iranian Society of Nephrology. The aim of the IJKD is the worldwide reflection of the knowledge produced by the scientists and clinicians in nephrology. Published quarterly, the IJKD provides a new platform for advancement of the field. The journal’s objective is to serve as a focal point for debates and exchange of knowledge and experience among researchers in a global context. Original papers, case reports, and invited reviews on all aspects of the kidney diseases, hypertension, dialysis, and transplantation will be covered by the IJKD. Research on the basic science, clinical practice, and socio-economics of renal health are all welcomed by the editors of the journal.
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