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电离辐射介导肺内不同组织学模式下细胞黏附分子的表达。

Ionizing radiation mediates expression of cell adhesion molecules in distinct histological patterns within the lung.

作者信息

Hallahan D E, Virudachalam S

机构信息

Department of Radiation and Cellular Oncology, University of Chicago and Pritzker School of Medicine, Illinois 60637, USA.

出版信息

Cancer Res. 1997 Jun 1;57(11):2096-9.

PMID:9187101
Abstract

Inflammatory cell infiltration of the lung is a predominant histopathological change that occurs during radiation pneumonitis. Emigration of inflammatory cells from the circulation requires the interaction between cell adhesion molecules on the vascular endothelium and molecules on the surface of leukocytes. We studied the immunohistochemical pattern of expression of cell adhesion molecules in lungs from mice treated with thoracic irradiation. After X-irradiation, the endothelial leukocyte adhesion molecule 1 (ELAM-1; E-selectin) was primarily expressed in the pulmonary endothelium of larger vessels and minimally in the microvascular endothelium. Conversely, the intercellular adhesion molecule 1 (ICAM-1; CD54) was expressed in the pulmonary capillary endothelium and minimally in the endothelium of larger vessels. Radiation-mediated E-selectin expression was first observed at 6 h, whereas ICAM-1 expression initially increased at 24 h after irradiation. ICAM-1 and E-selectin expression persisted for several days. P-selectin is constitutively expressed in Weibel-Palade bodies in the endothelium, which moved to the vascular lumen within 30 min after irradiation. P-selectin was not detected in the pulmonary endothelium at 6 h after irradiation. The radiation dose required for increased cell adhesion molecule expression within the pulmonary vascular endothelium was 2 Gy, and expression increased in a dose-dependent manner. These data demonstrate that ICAM-1 and E-selectin expression is increased in the pulmonary endothelium following thoracic irradiation. The pattern of expression of E-selectin, P-selectin, and ICAM-1 is distinct from one another.

摘要

肺部的炎性细胞浸润是放射性肺炎期间发生的主要组织病理学变化。炎性细胞从循环系统中渗出需要血管内皮细胞上的细胞黏附分子与白细胞表面分子之间的相互作用。我们研究了胸部照射小鼠肺部中细胞黏附分子表达的免疫组化模式。X线照射后,内皮白细胞黏附分子1(ELAM-1;E-选择素)主要在较大血管的肺内皮中表达,在微血管内皮中表达极少。相反,细胞间黏附分子1(ICAM-1;CD54)在肺毛细血管内皮中表达,在较大血管的内皮中表达极少。辐射介导的E-选择素表达在6小时首次观察到,而ICAM-1表达在照射后24小时开始增加。ICAM-1和E-选择素表达持续数天。P-选择素在内皮细胞的Weibel-Palade小体中组成性表达,照射后30分钟内转移至血管腔。照射后6小时在肺内皮中未检测到P-选择素。肺血管内皮中细胞黏附分子表达增加所需的辐射剂量为2 Gy,且表达呈剂量依赖性增加。这些数据表明,胸部照射后肺内皮中ICAM-1和E-选择素表达增加。E-选择素、P-选择素和ICAM-1的表达模式彼此不同。

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Ionizing radiation mediates expression of cell adhesion molecules in distinct histological patterns within the lung.电离辐射介导肺内不同组织学模式下细胞黏附分子的表达。
Cancer Res. 1997 Jun 1;57(11):2096-9.
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Cell adhesion molecules mediate radiation-induced leukocyte adhesion to the vascular endothelium.细胞黏附分子介导辐射诱导的白细胞与血管内皮的黏附。
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VEGF increases retinal vascular ICAM-1 expression in vivo.血管内皮生长因子(VEGF)在体内可增加视网膜血管细胞间黏附分子-1(ICAM-1)的表达。
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