Vitronectin and integrin vitronectin receptor localization in multiple sclerosis lesions.
Vitronectin and integrin vitronectin receptor localization in multiple sclerosis lesions.
复制标题
玻连蛋白和整合素玻连蛋白受体在多发性硬化症病变中的定位。
DOI：
10.1097/00005072-199503000-00007
复制
发表时间：
1995
影响因子：
3.2
通讯作者：
Hinojoza,JR
中科院分区：
文献类型：
--
作者：
Sobel,RA;Chen,M;Maeda,A;Hinojoza,JR
玻连蛋白（Vn）是一种多功能的血浆和细胞外基质糖蛋白，参与细胞粘附、凝血、吞噬以及保护旁观者细胞免受补体和T细胞介导的裂解。为确定多发性硬化症（MS）中枢神经系统（CNS）病变中Vn的定位位置以及表达整合素Vn受体的细胞可识别Vn的位置，对CNS组织样本进行Vn和αv、β1 n和β 3整合素Vn受体亚单位的免疫染色。通过光学和电子显微镜，Vn定位于活动性但非慢性病变、正常或其他神经系统疾病对照中的营养不良、脱髓鞘轴突内。这种定位与MS病变中的其他血浆蛋白不同，并且与在其他条件下发现的神经元细胞体定位模式不同。微血管Vn增加，少量反应性星形胶质细胞也呈Vn阳性。内皮细胞α v亚基的表达较对照组增加，β 1亚基的表达较对照组减少，而α v和β 1亚基均在活动性病变的巨噬细胞和胶质细胞上显著表达。β 3整合素亚基主要表达于血管内和血管周围的血小板上，在活动性斑块中以内皮细胞上表达更为明显。Vsituin的精确功能目前还不清楚。然而，这些结果表明，整合素Vn受体的表达调控是复杂的，并且随着MS病变的发展，Vn可能被识别并在不同的显微解剖部位具有多种功能。血管内Vn可参与凝血，从而促进白细胞外渗。实质Vn可激活T细胞和巨噬细胞或促进脱髓鞘。或者，Vn可能保护轴突免受损伤，从而有助于相对轴突保护，这是活动性MS病变的标志。
Vitronectin (Vn) is a multifunctional plasma and extracellular matrix glycoprotein involved in cell attachment, coagulation, phagocytosis, and the protection of bystander cells from complement- and T cell-mediated lysis. To determine where Vn is localized and where cells expressing integrin Vn receptors may recognize it in central nervous system (CNS) lesions of multiple sclerosis (MS), CNS tissue samples were immunostained for Vn and the αv, β1„, and β3integrin Vn receptor subunits. By light and electron microscopy, Vn was localized within dystrophic, demyelinated axons in active but not chronic lesions, normal or other neurologic disease controls. This localization is distinct from that of other plasma proteins in MS lesions and it differs from the pattern of neuron cell body localization found in other conditions. Microvascular Vn was increased and small numbers of reactive astrocytes were also Vn-positive in active plaques. Endothelial cell expression of the αvsubunit was increased over controls and that of the β1subunit was decreased whereas both the αvand β1subunits were prominently expressed on macrophages and glia in active lesions. The β3integrin subunit was expressed on platelets within and around vessels and was more prominent on endothelial cells in active plaques. The precise functions of Vnin situare not presently known. These results indicate, however, that the regulation of expression of integrin Vn receptors is complex and that Vn may be recognized and have multiple functions in different microanatomic sites as MS lesions evolve. Intravascular Vn could participate in clotting, thereby contributing to leukocyte extravasation. Parenchymal Vn could activate T cells and macrophages or promote demyelination. Alternatively, Vn might protect axons from injury, thereby contributing to relative axonal preservation, a hallmark of active MS lesions.