{"title":"内皮细胞粘附分子参与抗thy -1肾炎的发展。","authors":"Masato Isome, Hidehiko Fujinaka, Eishin Yaoita, Lili Feng, Laxman P Adhikary, Akira Abe, Satoko Tsuchida, Katsutoshi Kawasaki, Hitoshi Suzuki, Itaru Kihara, Curtis B Wilson, Tadashi Yamamoto","doi":"10.1159/000065298","DOIUrl":null,"url":null,"abstract":"<p><p>To study an involvement of glomerular endothelial cells in the development of anti-Thy-1 nephritis, we examined the expression of endothelial cell adhesion molecules during the course of this model. Ribonuclease protection assay elucidated that expression of mRNA for intercellular adhesion molecule-1 (ICAM-1) was markedly enhanced in the glomeruli with a peak at 2 h (6.5-fold, p < 0.05) after the anti-Thy-1 antibody injection when mesangial cell lysis was recognized and IL-1beta mRNA expression was induced in the glomeruli. The glomerular ICAM-1 was predominantly localized in the endothelial cells and was intensely immunostained at day 1 in the glomerular endothelial cells. In contrast, platelet endothelial cell adhesion molecule-1 (PECAM-1) and vascular endothelial-cadherin mRNA expression increased gradually with a peak at day 6 (2.6-fold (p < 0.05) and 4.2-fold (p < 0.05), respectively) in the glomeruli with mesangial proliferative lesion. PECAM-1 was also immunolocalized in the glomerular endothelial cells and the immunoreactivity was greatly enhanced at day 6. Glomerular expression of vascular cell adhesion molecule-1 and endothelial leukocyte adhesion molecule-1 (E-selectin) was unchanged at a low level during the course of anti-Thy-1 nephritis. Blocking of ICAM-1 by administration of anti-ICAM-1 antibody showed significant decrease in the number of polymorphonuclear leukocytes accumulating in the glomeruli by 45.7% (9.4 +/- 0.2 vs. 5.1 +/- 0.1 per glomerular cross section, p < 0.01) at 2 h. These results suggest a significant involvement of glomerular endothelial cells in the development and repair of anti-Thy-1 nephritis via direct or indirect intercellular interactions between mesangial cells and glomerular endothelial cells.</p>","PeriodicalId":12179,"journal":{"name":"Experimental nephrology","volume":"10 5-6","pages":"338-47"},"PeriodicalIF":0.0000,"publicationDate":"2002-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000065298","citationCount":"6","resultStr":"{\"title\":\"Involvement of endothelial cell adhesion molecules in the development of anti-Thy-1 nephritis.\",\"authors\":\"Masato Isome, Hidehiko Fujinaka, Eishin Yaoita, Lili Feng, Laxman P Adhikary, Akira Abe, Satoko Tsuchida, Katsutoshi Kawasaki, Hitoshi Suzuki, Itaru Kihara, Curtis B Wilson, Tadashi Yamamoto\",\"doi\":\"10.1159/000065298\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>To study an involvement of glomerular endothelial cells in the development of anti-Thy-1 nephritis, we examined the expression of endothelial cell adhesion molecules during the course of this model. Ribonuclease protection assay elucidated that expression of mRNA for intercellular adhesion molecule-1 (ICAM-1) was markedly enhanced in the glomeruli with a peak at 2 h (6.5-fold, p < 0.05) after the anti-Thy-1 antibody injection when mesangial cell lysis was recognized and IL-1beta mRNA expression was induced in the glomeruli. The glomerular ICAM-1 was predominantly localized in the endothelial cells and was intensely immunostained at day 1 in the glomerular endothelial cells. In contrast, platelet endothelial cell adhesion molecule-1 (PECAM-1) and vascular endothelial-cadherin mRNA expression increased gradually with a peak at day 6 (2.6-fold (p < 0.05) and 4.2-fold (p < 0.05), respectively) in the glomeruli with mesangial proliferative lesion. PECAM-1 was also immunolocalized in the glomerular endothelial cells and the immunoreactivity was greatly enhanced at day 6. Glomerular expression of vascular cell adhesion molecule-1 and endothelial leukocyte adhesion molecule-1 (E-selectin) was unchanged at a low level during the course of anti-Thy-1 nephritis. Blocking of ICAM-1 by administration of anti-ICAM-1 antibody showed significant decrease in the number of polymorphonuclear leukocytes accumulating in the glomeruli by 45.7% (9.4 +/- 0.2 vs. 5.1 +/- 0.1 per glomerular cross section, p < 0.01) at 2 h. These results suggest a significant involvement of glomerular endothelial cells in the development and repair of anti-Thy-1 nephritis via direct or indirect intercellular interactions between mesangial cells and glomerular endothelial cells.</p>\",\"PeriodicalId\":12179,\"journal\":{\"name\":\"Experimental nephrology\",\"volume\":\"10 5-6\",\"pages\":\"338-47\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2002-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.1159/000065298\",\"citationCount\":\"6\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Experimental nephrology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1159/000065298\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Experimental nephrology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000065298","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 6
摘要
为了研究肾小球内皮细胞在抗thy -1肾炎发生过程中的作用,我们检测了内皮细胞粘附分子在该模型过程中的表达。核糖核酸酶保护实验表明,在肾小球中识别系膜细胞裂解并诱导il -1 β mRNA表达时,抗hy-1抗体注射后2 h细胞间粘附分子-1 (ICAM-1) mRNA的表达明显增强,达到峰值(6.5倍,p < 0.05)。肾小球ICAM-1主要定位于内皮细胞,并在第1天在肾小球内皮细胞中出现强烈的免疫染色。血小板内皮细胞粘附分子-1 (PECAM-1)和血管内皮-钙粘蛋白mRNA表达逐渐升高,并在第6天达到峰值(分别为2.6倍(p < 0.05)和4.2倍(p < 0.05))。PECAM-1也在肾小球内皮细胞中免疫定位,免疫反应性在第6天显著增强。在抗thy -1肾炎过程中,肾小球血管细胞粘附分子-1和内皮白细胞粘附分子-1 (e-选择素)的表达在低水平下保持不变。通过抗ICAM-1抗体阻断ICAM-1,在2小时内,肾小球中积累的多形核白细胞数量显著减少45.7%(每肾小球横切面9.4 +/- 0.2 vs 5.1 +/- 0.1, p < 0.01)。这些结果表明,肾小球内皮细胞通过系膜细胞和肾小球内皮细胞之间的直接或间接的细胞间相互作用,显著参与了抗- ty -1肾炎的发展和修复。
Involvement of endothelial cell adhesion molecules in the development of anti-Thy-1 nephritis.
To study an involvement of glomerular endothelial cells in the development of anti-Thy-1 nephritis, we examined the expression of endothelial cell adhesion molecules during the course of this model. Ribonuclease protection assay elucidated that expression of mRNA for intercellular adhesion molecule-1 (ICAM-1) was markedly enhanced in the glomeruli with a peak at 2 h (6.5-fold, p < 0.05) after the anti-Thy-1 antibody injection when mesangial cell lysis was recognized and IL-1beta mRNA expression was induced in the glomeruli. The glomerular ICAM-1 was predominantly localized in the endothelial cells and was intensely immunostained at day 1 in the glomerular endothelial cells. In contrast, platelet endothelial cell adhesion molecule-1 (PECAM-1) and vascular endothelial-cadherin mRNA expression increased gradually with a peak at day 6 (2.6-fold (p < 0.05) and 4.2-fold (p < 0.05), respectively) in the glomeruli with mesangial proliferative lesion. PECAM-1 was also immunolocalized in the glomerular endothelial cells and the immunoreactivity was greatly enhanced at day 6. Glomerular expression of vascular cell adhesion molecule-1 and endothelial leukocyte adhesion molecule-1 (E-selectin) was unchanged at a low level during the course of anti-Thy-1 nephritis. Blocking of ICAM-1 by administration of anti-ICAM-1 antibody showed significant decrease in the number of polymorphonuclear leukocytes accumulating in the glomeruli by 45.7% (9.4 +/- 0.2 vs. 5.1 +/- 0.1 per glomerular cross section, p < 0.01) at 2 h. These results suggest a significant involvement of glomerular endothelial cells in the development and repair of anti-Thy-1 nephritis via direct or indirect intercellular interactions between mesangial cells and glomerular endothelial cells.