{"title":"抑制KCTD10通过降低VEGF和影响血管生成影响糖尿病视网膜病变的进展。","authors":"Yun Feng, Cong Wang, Guangwei Wang","doi":"10.1155/2022/4112307","DOIUrl":null,"url":null,"abstract":"<p><strong>Aim: </strong>We purposed to evaluate the KCTD10 effects of angiogenesis in diabetic retinopathy (DR).</p><p><strong>Methods: </strong>We induced a DR cell model using high glucose (HG) treatment of HRECs and ARPE-19 cells. A DR rat was established by injecting streptozotocin. Small interference RNA targeted KCTD10 (si-KCTD10) was used to mediate KCTD10 inhibition in cell and animal models. The roles of KCTD10 on cell viability, apoptosis, angiogenesis, and related proteins (VEGF and HIF-1<i>α</i>) were observed by RT-qPCR, Western blot, CCK-8 assay, TUNEL staining, tube formation assay, ELISA, and immunohistochemistry assay.</p><p><strong>Results: </strong>KCTD10 expression was upregulated in DR cells and retinal tissue of DR rats. Treatment of the cells with si-KCTD10 increased cell viability and decreased apoptosis and angiogenesis in DR cells. Inhibition of KCTD10 could reduce the expression of VEGF and HIF-1<i>α</i> in DR cells. Furthermore, KCTD10 inhibition reduced VEGF levels in the retinal tissue of DR rats.</p><p><strong>Conclusion: </strong>This work showed that inhibition of KCTD10 relieved angiogenesis in DR.</p>","PeriodicalId":12778,"journal":{"name":"Genetics research","volume":"2022 ","pages":"4112307"},"PeriodicalIF":1.4000,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9629933/pdf/","citationCount":"3","resultStr":"{\"title\":\"Inhibition of KCTD10 Affects Diabetic Retinopathy Progression by Reducing VEGF and Affecting Angiogenesis.\",\"authors\":\"Yun Feng, Cong Wang, Guangwei Wang\",\"doi\":\"10.1155/2022/4112307\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Aim: </strong>We purposed to evaluate the KCTD10 effects of angiogenesis in diabetic retinopathy (DR).</p><p><strong>Methods: </strong>We induced a DR cell model using high glucose (HG) treatment of HRECs and ARPE-19 cells. A DR rat was established by injecting streptozotocin. Small interference RNA targeted KCTD10 (si-KCTD10) was used to mediate KCTD10 inhibition in cell and animal models. The roles of KCTD10 on cell viability, apoptosis, angiogenesis, and related proteins (VEGF and HIF-1<i>α</i>) were observed by RT-qPCR, Western blot, CCK-8 assay, TUNEL staining, tube formation assay, ELISA, and immunohistochemistry assay.</p><p><strong>Results: </strong>KCTD10 expression was upregulated in DR cells and retinal tissue of DR rats. Treatment of the cells with si-KCTD10 increased cell viability and decreased apoptosis and angiogenesis in DR cells. Inhibition of KCTD10 could reduce the expression of VEGF and HIF-1<i>α</i> in DR cells. Furthermore, KCTD10 inhibition reduced VEGF levels in the retinal tissue of DR rats.</p><p><strong>Conclusion: </strong>This work showed that inhibition of KCTD10 relieved angiogenesis in DR.</p>\",\"PeriodicalId\":12778,\"journal\":{\"name\":\"Genetics research\",\"volume\":\"2022 \",\"pages\":\"4112307\"},\"PeriodicalIF\":1.4000,\"publicationDate\":\"2022-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9629933/pdf/\",\"citationCount\":\"3\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Genetics research\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1155/2022/4112307\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Genetics research","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1155/2022/4112307","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
Inhibition of KCTD10 Affects Diabetic Retinopathy Progression by Reducing VEGF and Affecting Angiogenesis.
Aim: We purposed to evaluate the KCTD10 effects of angiogenesis in diabetic retinopathy (DR).
Methods: We induced a DR cell model using high glucose (HG) treatment of HRECs and ARPE-19 cells. A DR rat was established by injecting streptozotocin. Small interference RNA targeted KCTD10 (si-KCTD10) was used to mediate KCTD10 inhibition in cell and animal models. The roles of KCTD10 on cell viability, apoptosis, angiogenesis, and related proteins (VEGF and HIF-1α) were observed by RT-qPCR, Western blot, CCK-8 assay, TUNEL staining, tube formation assay, ELISA, and immunohistochemistry assay.
Results: KCTD10 expression was upregulated in DR cells and retinal tissue of DR rats. Treatment of the cells with si-KCTD10 increased cell viability and decreased apoptosis and angiogenesis in DR cells. Inhibition of KCTD10 could reduce the expression of VEGF and HIF-1α in DR cells. Furthermore, KCTD10 inhibition reduced VEGF levels in the retinal tissue of DR rats.
Conclusion: This work showed that inhibition of KCTD10 relieved angiogenesis in DR.
期刊介绍：
Genetics Research is a key forum for original research on all aspects of human and animal genetics, reporting key findings on genomes, genes, mutations and molecular interactions, extending out to developmental, evolutionary, and population genetics as well as ethical, legal and social aspects. Our aim is to lead to a better understanding of genetic processes in health and disease. The journal focuses on the use of new technologies, such as next generation sequencing together with bioinformatics analysis, to produce increasingly detailed views of how genes function in tissues and how these genes perform, individually or collectively, in normal development and disease aetiology. The journal publishes original work, review articles, short papers, computational studies, and novel methods and techniques in research covering humans and well-established genetic organisms. Key subject areas include medical genetics, genomics, human evolutionary and population genetics, bioinformatics, genetics of complex traits, molecular and developmental genetics, Evo-Devo, quantitative and statistical genetics, behavioural genetics and environmental genetics. The breadth and quality of research make the journal an invaluable resource for medical geneticists, molecular biologists, bioinformaticians and researchers involved in genetic basis of diseases, evolutionary and developmental studies.
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