YunXia Wang, JiaJia Yang, Chun Wu, Yuqin Guo, Yuan Ding, Xiujuan Zou
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Potential targets of <i>SNHG14</i> were predicted using bioinformatics tools and verified by luciferase reporter, RNA pulldown, and northern blotting assays. The functional role of <i>SNHG14</i> in DN in vivo was detected by injection with adenoviral vector carrying sh-<i>SNHG14</i> into DN mice. Serum creatinine, blood urea nitrogen, blood glucose, 24-h proteinuria, relative kidney weight, and renal pathological changes were examined in DN mice.</p>\n </section>\n \n <section>\n \n <h3> Results</h3>\n \n <p><i>SNHG14</i> expression was elevated in the kidneys of DN mice and HG-treated MCs. <i>SNHG14</i> silencing inhibited proliferation and fibrosis of HG-stimulated MCs. <i>SNHG14</i> bound to <i>miR-30e-5p</i> to upregulate <i>SOX4</i> expression. In rescue assays, <i>SOX4</i> elevation diminished the effects of <i>SNHG14</i> silencing in HG-treated MCs, and <i>SOX4</i> silencing reversed the effects of <i>SNHG14</i> overexpression. In in vivo studies, <i>SNHG14</i> downregulation significantly ameliorated renal injuries and renal interstitial fibrosis in DN mice.</p>\n </section>\n \n <section>\n \n <h3> Conclusions</h3>\n \n <p><i>SNHG14</i> silencing attenuates kidney injury in DN mice and reduces proliferation and fibrotic phenotype of HG-stimulated MCs via the <i>miR-30e-5p</i>/<i>SOX4</i> axis.</p>\n \n <div>\n <figure>\n <div><picture>\n <source></source></picture><p></p>\n </div>\n </figure>\n </div>\n </section>\n </div>","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"16 6","pages":""},"PeriodicalIF":3.0000,"publicationDate":"2024-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.13565","citationCount":"0","resultStr":"{\"title\":\"LncRNA SNHG14 silencing attenuates the progression of diabetic nephropathy via the miR-30e-5p/SOX4 axis\",\"authors\":\"YunXia Wang, JiaJia Yang, Chun Wu, Yuqin Guo, Yuan Ding, Xiujuan Zou\",\"doi\":\"10.1111/1753-0407.13565\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<div>\\n \\n \\n <section>\\n \\n <h3> Background</h3>\\n \\n <p>Diabetic nephropathy (DN) is a diabetic complication. LncRNAs are reported to participate in the pathophysiology of DN. Here, the function and mechanism of lncRNA <i>small nucleolar RNA host gene</i> <i>14</i> (<i>SNHG14</i>) in DN were explored.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Methods</h3>\\n \\n <p>Streptozotocin (STZ)-induced DN mouse models and high glucose (HG)-treated human mesangial cells (MCs) were used to detect <i>SNHG14</i> expression. <i>SNHG14</i> silencing plasmids were applied to examine the function of <i>SNHG14</i> on proliferation and fibrosis in HG-treated MCs. Potential targets of <i>SNHG14</i> were predicted using bioinformatics tools and verified by luciferase reporter, RNA pulldown, and northern blotting assays. The functional role of <i>SNHG14</i> in DN in vivo was detected by injection with adenoviral vector carrying sh-<i>SNHG14</i> into DN mice. Serum creatinine, blood urea nitrogen, blood glucose, 24-h proteinuria, relative kidney weight, and renal pathological changes were examined in DN mice.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Results</h3>\\n \\n <p><i>SNHG14</i> expression was elevated in the kidneys of DN mice and HG-treated MCs. <i>SNHG14</i> silencing inhibited proliferation and fibrosis of HG-stimulated MCs. <i>SNHG14</i> bound to <i>miR-30e-5p</i> to upregulate <i>SOX4</i> expression. In rescue assays, <i>SOX4</i> elevation diminished the effects of <i>SNHG14</i> silencing in HG-treated MCs, and <i>SOX4</i> silencing reversed the effects of <i>SNHG14</i> overexpression. In in vivo studies, <i>SNHG14</i> downregulation significantly ameliorated renal injuries and renal interstitial fibrosis in DN mice.</p>\\n </section>\\n \\n <section>\\n \\n <h3> Conclusions</h3>\\n \\n <p><i>SNHG14</i> silencing attenuates kidney injury in DN mice and reduces proliferation and fibrotic phenotype of HG-stimulated MCs via the <i>miR-30e-5p</i>/<i>SOX4</i> axis.</p>\\n \\n <div>\\n <figure>\\n <div><picture>\\n <source></source></picture><p></p>\\n </div>\\n </figure>\\n </div>\\n </section>\\n </div>\",\"PeriodicalId\":189,\"journal\":{\"name\":\"Journal of Diabetes\",\"volume\":\"16 6\",\"pages\":\"\"},\"PeriodicalIF\":3.0000,\"publicationDate\":\"2024-05-16\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.13565\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Diabetes\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1111/1753-0407.13565\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Diabetes","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1111/1753-0407.13565","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
LncRNA SNHG14 silencing attenuates the progression of diabetic nephropathy via the miR-30e-5p/SOX4 axis
Background
Diabetic nephropathy (DN) is a diabetic complication. LncRNAs are reported to participate in the pathophysiology of DN. Here, the function and mechanism of lncRNA small nucleolar RNA host gene14 (SNHG14) in DN were explored.
Methods
Streptozotocin (STZ)-induced DN mouse models and high glucose (HG)-treated human mesangial cells (MCs) were used to detect SNHG14 expression. SNHG14 silencing plasmids were applied to examine the function of SNHG14 on proliferation and fibrosis in HG-treated MCs. Potential targets of SNHG14 were predicted using bioinformatics tools and verified by luciferase reporter, RNA pulldown, and northern blotting assays. The functional role of SNHG14 in DN in vivo was detected by injection with adenoviral vector carrying sh-SNHG14 into DN mice. Serum creatinine, blood urea nitrogen, blood glucose, 24-h proteinuria, relative kidney weight, and renal pathological changes were examined in DN mice.
Results
SNHG14 expression was elevated in the kidneys of DN mice and HG-treated MCs. SNHG14 silencing inhibited proliferation and fibrosis of HG-stimulated MCs. SNHG14 bound to miR-30e-5p to upregulate SOX4 expression. In rescue assays, SOX4 elevation diminished the effects of SNHG14 silencing in HG-treated MCs, and SOX4 silencing reversed the effects of SNHG14 overexpression. In in vivo studies, SNHG14 downregulation significantly ameliorated renal injuries and renal interstitial fibrosis in DN mice.
Conclusions
SNHG14 silencing attenuates kidney injury in DN mice and reduces proliferation and fibrotic phenotype of HG-stimulated MCs via the miR-30e-5p/SOX4 axis.
期刊介绍：
Journal of Diabetes (JDB) devotes itself to diabetes research, therapeutics, and education. It aims to involve researchers and practitioners in a dialogue between East and West via all aspects of epidemiology, etiology, pathogenesis, management, complications and prevention of diabetes, including the molecular, biochemical, and physiological aspects of diabetes. The Editorial team is international with a unique mix of Asian and Western participation.
The Editors welcome submissions in form of original research articles, images, novel case reports and correspondence, and will solicit reviews, point-counterpoint, commentaries, editorials, news highlights, and educational content.
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