PDF(Pubmed)
Abstract：
UNASSIGNED: Age-related macular degeneration (AMD) is the leading cause of blindness, and is associated with oxidative stress and the development of new blood vessels. At present, the main clinical treatment for AMD includes intraocular injection of vascular endothelial growth factor (VEGF). However, treatment includes repeated injections with significant side-effects. Therefore, new treatment options are required. The aim of the present study was to discover the new treatment target of AMD from the gene level.
UNASSIGNED: The Gene Expression Omnibus (GEO) database was used to analyze the differential gene expression in AMD, and the regulator of G-protein signaling 1 (RGS1) was obtained by bioassay. Western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were used to detect the expression levels of RGS1, VEGF, and other related molecules in human microvascular endothelial cells (HMECs) under different conditions. Cell viability, apoptosis, and proliferation of HMECs were measured by Cell Counting Kit-8 proliferation assay. Immunofluorescence and immunohistochemistry detected the interaction between RGS1, platelet endothelial cell adhesion molecule-1, and VEGF.
UNASSIGNED: RGS1 was found to closely associated with the proliferation of vascular endothelial cells, and therefore, with angiogenesis. The expression of RGS1, VEGF, and platelet endothelial cell adhesion molecule-1 was upregulated in laser model mice and hypoxia model HMECs. Knockout of RGS1 inhibits the expression of VEGF and HMEC proliferation, thereby inhibiting AMD angiogenesis.
UNASSIGNED: Our results support the use of RGS1 as a new potential target for the future treatment of AMD.
UNASSIGNED: The Gene Expression Omnibus (GEO) database was used to analyze the differential gene expression in AMD, and the regulator of G-protein signaling 1 (RGS1) was obtained by bioassay. Western blotting and quantitative reverse transcription polymerase chain reaction (qRT-PCR) were used to detect the expression levels of RGS1, VEGF, and other related molecules in human microvascular endothelial cells (HMECs) under different conditions. Cell viability, apoptosis, and proliferation of HMECs were measured by Cell Counting Kit-8 proliferation assay. Immunofluorescence and immunohistochemistry detected the interaction between RGS1, platelet endothelial cell adhesion molecule-1, and VEGF.
UNASSIGNED: RGS1 was found to closely associated with the proliferation of vascular endothelial cells, and therefore, with angiogenesis. The expression of RGS1, VEGF, and platelet endothelial cell adhesion molecule-1 was upregulated in laser model mice and hypoxia model HMECs. Knockout of RGS1 inhibits the expression of VEGF and HMEC proliferation, thereby inhibiting AMD angiogenesis.
UNASSIGNED: Our results support the use of RGS1 as a new potential target for the future treatment of AMD.
摘要：
未经证实：年龄相关性黄斑变性（AMD）是导致失明的主要原因，并与氧化应激和新血管的发育有关。目前,临床治疗AMD主要包括眼内注射血管内皮生长因子(VEGF)。然而,治疗包括重复注射，有明显的副作用。因此,需要新的治疗方案。本研究旨在从基因水平上发现AMD新的治疗靶点。
UNASSIGNED：基因表达综合（GEO）数据库用于分析AMD中的差异基因表达，并通过生物测定获得G蛋白信号调节因子1（RGS1）。免疫印迹和定量逆转录聚合酶链反应(qRT-PCR)检测RGS1、VEGF、和其他相关分子在不同条件下的人微血管内皮细胞（HMEC）。细胞活力，凋亡，和HMEC的增殖通过细胞计数试剂盒-8增殖测定来测量。免疫荧光和免疫组织化学检测RGS1、血小板内皮细胞粘附分子-1和VEGF之间的相互作用。
未经证实：发现RGS1与血管内皮细胞的增殖密切相关，因此,血管生成。RGS1、VEGF的表达,血小板内皮细胞粘附分子-1在激光模型小鼠和缺氧模型HMEC中表达上调。RGS1基因敲除抑制VEGF表达和HMEC增殖,从而抑制AMD血管生成。
UNASSIGNED：我们的结果支持使用RGS1作为未来治疗AMD的新的潜在靶标。
UNASSIGNED：基因表达综合（GEO）数据库用于分析AMD中的差异基因表达，并通过生物测定获得G蛋白信号调节因子1（RGS1）。免疫印迹和定量逆转录聚合酶链反应(qRT-PCR)检测RGS1、VEGF、和其他相关分子在不同条件下的人微血管内皮细胞（HMEC）。细胞活力，凋亡，和HMEC的增殖通过细胞计数试剂盒-8增殖测定来测量。免疫荧光和免疫组织化学检测RGS1、血小板内皮细胞粘附分子-1和VEGF之间的相互作用。
未经证实：发现RGS1与血管内皮细胞的增殖密切相关，因此,血管生成。RGS1、VEGF的表达,血小板内皮细胞粘附分子-1在激光模型小鼠和缺氧模型HMEC中表达上调。RGS1基因敲除抑制VEGF表达和HMEC增殖,从而抑制AMD血管生成。
UNASSIGNED：我们的结果支持使用RGS1作为未来治疗AMD的新的潜在靶标。
