Comparative analysis of the expression patterns of various TNFSF/TNFRSF in atherosclerotic plaques.
Members of the TNFSF/TNFRSF are involved in the immunoregulation of various immune reactions and diseases. Recently, LIGHT/TR2, GITRL/GITR, and TL1A/DR3 have been reported as playing roles in the inflammatory reactions in atherosclerosis, but a comparative analysis of these molecules has not been conducted. In order to compare their expression patterns, immunohistochemical analyses were performed using six human carotid endoarterectomy samples. The expression of these molecules was detected in the various cell types that constitute atherosclerotic plaques. The expression of all analyzed molecules was detected, albeit at various levels, mainly in foamy macrophages in all tested samples. The strong expression of these molecules in endothelial and smooth muscle cells was also detected in 2 and 1 plaque samples, respectively, while others express only some of the tested molecules. Flow cytometry analyses of human monocyte/macrophage cell lines, U937 and THP-1, detected the expression of the tested molecules while a relatively undifferentiated monocytic cell line, TF-1A, failed to express them. These data indicate that activated and differentiated macrophages are the main cell type expressing tested molecules in atherosclerotic plaques while endothelial and smooth muscle cells can express them in limited cases. Pro-inflammatory activities of the tested molecules may contribute to the atherogenesis by stimulating the cells expressing them in atherosclerotic plaques and the successful treatment of atherosclerosis may require cooperative regulation of these activities.
Department of Genetic Engineering, School of Life Sciences and Biotechnology School of Medicine, Kyungpook National University, Daegu, Korea.
Won-Jung
WJ
Kim
Yoon-Joong
YJ
Kang
Kyoungho
K
Suk
Jeong-Euy
JE
Park
Byoung S
BS
Kwon
Won-Ha
WH
Lee
D050197:Atherosclerosis / Q000276:immunology* / Q000378:metabolism; D002460:Cell Line; D045744:Cell Line, Tumor; D015870:Gene Expression; D053450:Glucocorticoid-Induced TNFR-Related Protein; D006801:Humans; D008024:Ligands; D008264:Macrophages / Q000276:immunology* / Q000378:metabolism; D017475:Receptors, Nerve Growth Factor / Q000378:metabolism; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D053240:Receptors, Tumor Necrosis Factor, Member 14 / Q000378:metabolism; D053219:Receptors, Tumor Necrosis Factor, Member 25 / Q000378:metabolism; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14 / Q000378:metabolism; D053380:Tumor Necrosis Factor Ligand Superfamily Member 15 / Q000378:metabolism; D048069:Tumor Necrosis Factors / Q000378:metabolism*
D053450:Glucocorticoid-Induced TNFR-Related Protein; D008024:Ligands; D017475:Receptors, Nerve Growth Factor; D018124:Receptors, Tumor Necrosis Factor; D053240:Receptors, Tumor Necrosis Factor, Member 14; D053219:Receptors, Tumor Necrosis Factor, Member 25; C491405:TNFRSF18 protein, human; C506033:TNFRSF25 protein, human; C505914:TNFSF14 protein, human; C117026:TNFSF15 protein, human; C478967:TNFSF18 protein, human; D053326:Tumor Necrosis Factor Ligand Superfamily Member 14; D053380:Tumor Necrosis Factor Ligand Superfamily Member 15; D048069:Tumor Necrosis Factors