Molecular mechanisms of and novel pathomorphological bases on vasculitis syndromes

血管细胞生物学的最新进展可能有助于阐明血管炎综合征的分子机制和病理形态学基础。因此，我们进行了几个项目，以进行如下的新转向血管细胞表型表达的分子病理分析1)血管炎中细胞与分子间的交叉对话（粘附分子、组胺、NO、凋亡、血管重构），2)血管生成（基因表达、FGF-2/VEGF、内皮细胞分化新途径、三维分析），3)疾病特异性病理形态学特征(IAAA、肺丛状血管病、Takayasu动脉炎、MPA、胶原病肝内血管炎、动脉硬化、血管损伤中宿主因子的影响和调节：1) ANCA（血管损伤机制、血管炎组织分布、肾小球病变规律变化、高松动脉炎），2)血清因子（抗内皮细胞抗体、rheu…More matoid因子、抗磷脂综合征、内皮细胞可吞噬抗体），3)T细胞克隆（GCA、病理生理动力学、高松动脉炎、动脉硬化），4)溶酶体酶（川崎病），3血管炎动物模型：1)川asaki病（白色假丝酵素提取物诱导的血管炎，MPO-敲除小鼠），2)病毒依赖性血管炎（HTLV-1 env-pX转基因大鼠，HCMV-IE转基因小鼠），3)胶原病血管炎MRL小鼠（IRF-1转基因抑制和趋化因子拮抗剂基因转移），4基因组分析：1)高松动脉炎（HLA多态性，lKBL1 SNP）， 2)地理病理学（高松动脉炎），3)MRL小鼠血管炎（定位候选基因，血管径特异性基因位点，35个血管炎研究的重组近交系），4)川崎病模型小鼠（血管炎耐药基因位点），5 .“2000年全体性血管炎国际研讨会”，东京，2000年10月14日，2)“血管炎研究的新进展”，松山，2002年2月16日。少

Recent advances in vascular cell biology may make it possible to clarify the molecular mechanisms and pathomorphological bases of vasculitis syndromes. We thus performed several projects to take a new turn as follows.1 Molecular pathological analyses of the phenotypic expression of vascular cells: 1) cross talks among cells and molecules in vasculitis (adhesion molecules, histamine, NO, apoptosis, vascular remodeling), 2) angiogenesis (gene expression, FGF-2/VEGF, a new differentiation pathway of endothelial cells, three dimensional analysis), 3) pathomorphological features specific for diseases (IAAA, pulmonary plexiform angiopathy, Takayasu arteritis, MPA, intra-hepatic vasculitis in collagen disease, arteriosclerosis, vasa-vasoritis),2 Affecting and modifying host factors in vascular injury: 1) ANCA (mechanisms of vascular injury, tissue distribution of vasculitis, regular variations of glomerular lesions, Takayasu arteritis), 2) serum factors (anti-endothelial cell antibodies, rheu … More matoid factors, anti-phospholipid syndrome, antibodies phagocytizable by endothelial cells), 3) T cell clonalities (GCA, pathophysiological dymanics, Takayasu arteritis, arteriosclerosis), 4) lysosomal enzymes (Kawasaki disease),3 Animal models for vasculitis: 1) Kawasaki disease (C.albicans extract-induced vasculitis, MPO- knock out mice), 2) Virus-dependent vasculitis (HTLV-1 env-pX transgenic rat, HCMV-IE transgenic mice), 3) MRL mice for vasculitis in collagen disease (inhibition by IRF-1 trans gene and gene transfer of chemokine antagonist),4 Genome analysis: 1) Takayasu arteritis (HLA polymorphism, SNP of lKBL1), 2) geographical pathology (Takayasu arteritis), 3) MRL mouse vasculitis (positional candidate genes, blood vessel-caliber specific gene loci, 35 recombinat inbred strains for vasculitis research), 4) Kawasaki disease model mice (vasculitis-resistant loci),5 Extramural seminars: 1) "International Workshop on Systemic Vasculitis 2000", Tokyo, Oct. 14, 2000, 2) "New Developments in Vasculitis Research", Matsuyama, Feb. 16, 2002. Less