公开(公告)号：US20040229796A1

公开(公告)日：2004-11-18

申请号：US10786223

申请日：2004-02-23

申请人： Maine Medical Center Research Institute

发明人： Thomas Maciag ,  Anna Mandinova ,  Lazar Mandinov ,  Igor Prudovsky ,  Stephen Bellum ,  Raffaella Soldi ,  Cinzia Bagala

IPC分类号： A61K038/17 ,  A61K031/555 ,  A61K031/195

CPC分类号： G01N33/6863 ,  A61K31/195 ,  A61K31/28 ,  A61K31/355 ,  A61K33/34 ,  A61K38/1738 ,  A61K45/06 ,  G01N33/6869 ,  G01N2333/545 ,  G01N2500/10

摘要： The present invention relates to the discovery that non-traditional export of certain pro-inflammatory cytokines lacking a signal sequence from a cell can be inhibited by copper chelation and/or administration to the cell of a truncated form of S100A13 lacking the basic residue portion. Further, copper chelation inhibits, inter alia, neointima formation, macrophage infiltration and associated inflammation, cell proliferation, secretion of extracellular matrix, intimal thickening, adventitial angiogenesis, restenosis, and the like, associated with vascular vessel injury. Thus, the present invention provides novel methods of preventing and treating, and for identifying novel compounds also useful as therapeutics for, such conditions.

摘要翻译： 本发明涉及以下发现：通过对缺乏碱性残基部分的S100A13截短形式的细胞进行铜螯合和/或给药，可以抑制某些缺乏来自细胞的信号序列的促炎细胞因子的非传统出口。 此外，铜螯合尤其抑制与血管损伤相关的新内膜形成，巨噬细胞浸润和相关炎症，细胞增殖，分泌细胞外基质，内膜增厚，外膜血管生成，再狭窄等。 因此，本发明提供了预防和治疗以及用于鉴定也可用作这些病症的治疗剂的新化合物的新方法。