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1. 发明申请

WO2011008641A1 METHIDS OF MODULATING ANGIOGENESIS AND TREATMENT OF ANGIOGENESIS-RELATED DISEASES 审中-公开
标题翻译：调节血管发生和治疗血管发生相关疾病的甲状腺
公开(公告)号：WO2011008641A1
公开(公告)日：2011-01-20
申请号：PCT/US2010/041484
申请日：2010-07-09
申请人： BETH ISRAEL DEACONESS MEDICAL CENTER, INC. , AN, Xiaojin , LI, Jian
发明人： AN, Xiaojin , LI, Jian
IPC分类号： C07K14/47 , C12N15/113
CPC分类号： C07K14/4702 , C07K14/82 , C12N15/113 , C12N15/1135 , C12N2310/11 , C12N2310/14 , C12N2310/3181 , C12N2310/3233
摘要： The present invention relates to a novel function for RGC-32 as an inhibitor of angiogenesis and a mediator between VEGF and FGF2 pathways. The present invention provides that expression of RGC-32 is induced in endothelial cells under hypoxia and that overexpression of RGC-32 in endothelial cells inhibited endothelial cell proliferation and migration via downregulation of another major angiogenic protein, FGF2, to further effect cyclin E. Also, RGC-32 promoted unstable vascular structure by increasing the numbers of apoptotic cells. The present invention provides methods of inhibiting proliferation of endothelial cells, angiogenesis, tumor growth by increasing expression of RGC-32 in the endothelial cells. The present invention relates to methods of increasing proliferation of endothelial cells as well as methods of treating ischemia by inhibiting expression of RGC-32 in the endothelial cells.
摘要翻译：本发明涉及RGC-32作为血管生成抑制剂和VEGF与FGF2途径之间介导的新功能。本发明提供了在缺氧下内皮细胞中诱导RGC-32的表达，并且内皮细胞中RGC-32的过度表达通过下调另一种主要血管生成蛋白FGF2来抑制内皮细胞增殖和迁移，从而进一步影响细胞周期蛋白E. RGC-32通过增加凋亡细胞的数量来促进血管结构的不稳定。本发明提供通过增加内皮细胞中RGC-32的表达来抑制内皮细胞增殖，血管发生，肿瘤生长的方法。本发明涉及通过抑制内皮细胞中RGC-32的表达来增加内皮细胞增殖的方法以及治疗缺血的方法。

2. 发明申请

WO2011008641A8 METHODS OF MODULATING ANGIOGENESIS AND TREATMENT OF ANGIOGENESIS-RELATED DISEASES 审中-公开
标题翻译：调节血管发生和治疗血管发生相关疾病的方法
公开(公告)号：WO2011008641A8
公开(公告)日：2011-03-31
申请号：PCT/US2010041484
申请日：2010-07-09
申请人： BETH ISRAEL HOSPITAL , AN XIAOJIN , LI JIAN
发明人： AN XIAOJIN , LI JIAN
IPC分类号： C07K14/47 , C12N15/113
CPC分类号： C07K14/4702 , C07K14/82 , C12N15/113 , C12N15/1135 , C12N2310/11 , C12N2310/14 , C12N2310/3181 , C12N2310/3233
摘要： The present invention relates to a novel function for RGC-32 as an inhibitor of angiogenesis and a mediator between VEGF and FGF2 pathways. The present invention provides that expression of RGC-32 is induced in endothelial cells under hypoxia and that overexpression of RGC-32 in endothelial cells inhibited endothelial cell proliferation and migration via downregulation of another major angiogenic protein, FGF2, to further effect cyclin E. Also, RGC-32 promoted unstable vascular structure by increasing the numbers of apoptotic cells. The present invention provides methods of inhibiting proliferation of endothelial cells, angiogenesis, tumor growth by increasing expression of RGC-32 in the endothelial cells. The present invention relates to methods of increasing proliferation of endothelial cells as well as methods of treating ischemia by inhibiting expression of RGC-32 in the endothelial cells.
摘要翻译：本发明涉及RGC-32作为血管生成抑制剂和VEGF与FGF2途径之间介导的新功能。本发明提供了在缺氧下内皮细胞中诱导RGC-32的表达，并且内皮细胞中RGC-32的过度表达通过下调另一种主要血管生成蛋白FGF2来抑制内皮细胞增殖和迁移，从而进一步影响细胞周期蛋白E. RGC-32通过增加凋亡细胞的数量来促进血管结构的不稳定。本发明提供通过增加内皮细胞中RGC-32的表达来抑制内皮细胞增殖，血管发生，肿瘤生长的方法。本发明涉及通过抑制内皮细胞中RGC-32的表达来增加内皮细胞增殖的方法以及治疗缺血的方法。

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