Inhibition of KCTD10 Affects Diabetic Retinopathy Progression by Reducing VEGF and Affecting Angiogenesis.

IF 1.4 4区生物学 Q4 GENETICS & HEREDITY

Genetics research Pub Date : 2022-01-01 DOI:10.1155/2022/4112307

Yun Feng, Cong Wang, Guangwei Wang

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引用次数: 3

Abstract

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.

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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。

目的:探讨KCTD10在糖尿病视网膜病变(DR)血管生成中的作用。方法:采用高糖(HG)处理HRECs和ARPE-19细胞，建立DR细胞模型。用链脲佐菌素建立DR大鼠。小干扰RNA靶向KCTD10 (si-KCTD10)在细胞和动物模型中介导KCTD10抑制。采用RT-qPCR、Western blot、CCK-8、TUNEL染色、成管实验、ELISA、免疫组化等方法观察KCTD10对细胞活力、凋亡、血管生成及相关蛋白(VEGF、HIF-1α)的影响。结果:KCTD10在DR大鼠视网膜组织和DR细胞中表达上调。用si-KCTD10处理细胞可提高细胞活力，减少细胞凋亡和血管生成。抑制KCTD10可降低DR细胞中VEGF和HIF-1α的表达。此外，KCTD10抑制降低了DR大鼠视网膜组织中的VEGF水平。结论:抑制KCTD10可缓解DR血管生成。

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来源期刊

Genetics research 生物-遗传学

自引率

6.70%

发文量

审稿时长

>12 weeks

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.