Antibody Binding to Fas Ligand Attenuates Inflammatory Cell Infiltration and Cytokine Secretion, Leading to Reduction of Myocardial Infarct Areas and Reperfusion Injury
Fas ligand (FasL) induces apoptotic cell death when bound to Fas antigen. The engagement of FasL has anti-inflammatory effects through the prevention of cell proliferation and cytokine secretion. However, the role of FasL in myocardial ischemia/reperfusion (MI/R) injury is unclear. We examined the e...
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| Veröffentlicht in: | Laboratory investigation 2002-09, Vol.82 (9), p.1121-1129 |
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| creator | Shiraishi, Hirokazu Toyozaki, Tetsuya Tsukamoto, Yoshiaki Saito, Toshihiro Masuda, Yoshiaki Hiroshima, Kenzo Ohwada, Hidemi Kobayashi, Nobuyuki Hiroe, Michiaki |
| description | Fas ligand (FasL) induces apoptotic cell death when bound to Fas antigen. The engagement of FasL has anti-inflammatory effects through the prevention of cell proliferation and cytokine secretion. However, the role of FasL in myocardial ischemia/reperfusion (MI/R) injury is unclear. We examined the expression of FasL mRNA in the myocardium of MI/R rats by ligating the left coronary artery for 30 minutes and allowing reperfusion to occur for 0, 1, 3, and 24 hours. The expression of FasL mRNA was enhanced 1 hour after reperfusion, and enhanced levels were consistently seen after 24 hours of reperfusion. FasL immunostaining was observed on neutrophils, macrophages, T cells, and vascular endothelial cells. We then assessed the potential role of FasL in the cell proliferation and cytokine production seen in MI/R injury after 24 hours of reperfusion. Rats were divided into three groups; Group A, without treatment; Group B, treated with nonspecific rabbit IgG; and Group C, treated with anti-FasL antibody. Anti-FasL antibody or rabbit IgG were administered intravenously before coronary artery occlusion. In Group C, interleukin-1β and interleukin-2 mRNA levels were decreased, and neutrophil and T cell accumulation was attenuated. The infarct area determined by triphenyltetrazolium chloride staining was significantly smaller in Group C (18 ± 4%) than in Group A (34 ± 2%) or Group B (33 ± 4%) (p < 0.0001). However, there was no significant difference in the prevalence of terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling-positive cardiomyocytes among the three groups. These findings suggest that the cardioprotective effect of anti-FasL antibody is due to its anti-inflammatory action, rather than antiapoptotic action. The Fas/FasL system may be involved in the development of MI/R injury. |
| doi_str_mv | 10.1097/01.LAB.0000029148.88524.CE |
| format | Article |
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The engagement of FasL has anti-inflammatory effects through the prevention of cell proliferation and cytokine secretion. However, the role of FasL in myocardial ischemia/reperfusion (MI/R) injury is unclear. We examined the expression of FasL mRNA in the myocardium of MI/R rats by ligating the left coronary artery for 30 minutes and allowing reperfusion to occur for 0, 1, 3, and 24 hours. The expression of FasL mRNA was enhanced 1 hour after reperfusion, and enhanced levels were consistently seen after 24 hours of reperfusion. FasL immunostaining was observed on neutrophils, macrophages, T cells, and vascular endothelial cells. We then assessed the potential role of FasL in the cell proliferation and cytokine production seen in MI/R injury after 24 hours of reperfusion. Rats were divided into three groups; Group A, without treatment; Group B, treated with nonspecific rabbit IgG; and Group C, treated with anti-FasL antibody. Anti-FasL antibody or rabbit IgG were administered intravenously before coronary artery occlusion. In Group C, interleukin-1β and interleukin-2 mRNA levels were decreased, and neutrophil and T cell accumulation was attenuated. The infarct area determined by triphenyltetrazolium chloride staining was significantly smaller in Group C (18 ± 4%) than in Group A (34 ± 2%) or Group B (33 ± 4%) (p < 0.0001). However, there was no significant difference in the prevalence of terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling-positive cardiomyocytes among the three groups. These findings suggest that the cardioprotective effect of anti-FasL antibody is due to its anti-inflammatory action, rather than antiapoptotic action. The Fas/FasL system may be involved in the development of MI/R injury.</description><identifier>ISSN: 0023-6837</identifier><identifier>EISSN: 1530-0307</identifier><identifier>DOI: 10.1097/01.LAB.0000029148.88524.CE</identifier><identifier>PMID: 12218072</identifier><identifier>CODEN: LAINAW</identifier><language>eng</language><publisher>New York: Elsevier Inc</publisher><subject>Animals ; Antibodies - therapeutic use ; Apoptosis ; Biological and medical sciences ; Cardiovascular system ; Chemokine CCL2 - physiology ; Cytokines - biosynthesis ; Fas Ligand Protein ; Laboratory Medicine ; Male ; Medical sciences ; Medicine ; Medicine & Public Health ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - immunology ; Membrane Glycoproteins - physiology ; Miscellaneous ; Myocardial Infarction - immunology ; Myocardial Infarction - pathology ; Myocardial Infarction - therapy ; Myocardial Reperfusion Injury - prevention & control ; Neutrophils - physiology ; Pathology ; Pharmacology. 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The engagement of FasL has anti-inflammatory effects through the prevention of cell proliferation and cytokine secretion. However, the role of FasL in myocardial ischemia/reperfusion (MI/R) injury is unclear. We examined the expression of FasL mRNA in the myocardium of MI/R rats by ligating the left coronary artery for 30 minutes and allowing reperfusion to occur for 0, 1, 3, and 24 hours. The expression of FasL mRNA was enhanced 1 hour after reperfusion, and enhanced levels were consistently seen after 24 hours of reperfusion. FasL immunostaining was observed on neutrophils, macrophages, T cells, and vascular endothelial cells. We then assessed the potential role of FasL in the cell proliferation and cytokine production seen in MI/R injury after 24 hours of reperfusion. Rats were divided into three groups; Group A, without treatment; Group B, treated with nonspecific rabbit IgG; and Group C, treated with anti-FasL antibody. Anti-FasL antibody or rabbit IgG were administered intravenously before coronary artery occlusion. In Group C, interleukin-1β and interleukin-2 mRNA levels were decreased, and neutrophil and T cell accumulation was attenuated. The infarct area determined by triphenyltetrazolium chloride staining was significantly smaller in Group C (18 ± 4%) than in Group A (34 ± 2%) or Group B (33 ± 4%) (p < 0.0001). However, there was no significant difference in the prevalence of terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling-positive cardiomyocytes among the three groups. These findings suggest that the cardioprotective effect of anti-FasL antibody is due to its anti-inflammatory action, rather than antiapoptotic action. The Fas/FasL system may be involved in the development of MI/R injury.</description><subject>Animals</subject><subject>Antibodies - therapeutic use</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Cardiovascular system</subject><subject>Chemokine CCL2 - physiology</subject><subject>Cytokines - biosynthesis</subject><subject>Fas Ligand Protein</subject><subject>Laboratory Medicine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Membrane Glycoproteins - immunology</subject><subject>Membrane Glycoproteins - physiology</subject><subject>Miscellaneous</subject><subject>Myocardial Infarction - immunology</subject><subject>Myocardial Infarction - pathology</subject><subject>Myocardial Infarction - therapy</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Neutrophils - physiology</subject><subject>Pathology</subject><subject>Pharmacology. 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The engagement of FasL has anti-inflammatory effects through the prevention of cell proliferation and cytokine secretion. However, the role of FasL in myocardial ischemia/reperfusion (MI/R) injury is unclear. We examined the expression of FasL mRNA in the myocardium of MI/R rats by ligating the left coronary artery for 30 minutes and allowing reperfusion to occur for 0, 1, 3, and 24 hours. The expression of FasL mRNA was enhanced 1 hour after reperfusion, and enhanced levels were consistently seen after 24 hours of reperfusion. FasL immunostaining was observed on neutrophils, macrophages, T cells, and vascular endothelial cells. We then assessed the potential role of FasL in the cell proliferation and cytokine production seen in MI/R injury after 24 hours of reperfusion. Rats were divided into three groups; Group A, without treatment; Group B, treated with nonspecific rabbit IgG; and Group C, treated with anti-FasL antibody. Anti-FasL antibody or rabbit IgG were administered intravenously before coronary artery occlusion. In Group C, interleukin-1β and interleukin-2 mRNA levels were decreased, and neutrophil and T cell accumulation was attenuated. The infarct area determined by triphenyltetrazolium chloride staining was significantly smaller in Group C (18 ± 4%) than in Group A (34 ± 2%) or Group B (33 ± 4%) (p < 0.0001). However, there was no significant difference in the prevalence of terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling-positive cardiomyocytes among the three groups. These findings suggest that the cardioprotective effect of anti-FasL antibody is due to its anti-inflammatory action, rather than antiapoptotic action. The Fas/FasL system may be involved in the development of MI/R injury.</abstract><cop>New York</cop><pub>Elsevier Inc</pub><pmid>12218072</pmid><doi>10.1097/01.LAB.0000029148.88524.CE</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antibodies - therapeutic use Apoptosis Biological and medical sciences Cardiovascular system Chemokine CCL2 - physiology Cytokines - biosynthesis Fas Ligand Protein Laboratory Medicine Male Medical sciences Medicine Medicine & Public Health Membrane Glycoproteins - genetics Membrane Glycoproteins - immunology Membrane Glycoproteins - physiology Miscellaneous Myocardial Infarction - immunology Myocardial Infarction - pathology Myocardial Infarction - therapy Myocardial Reperfusion Injury - prevention & control Neutrophils - physiology Pathology Pharmacology. Drug treatments Rats Rats, Sprague-Dawley RNA, Messenger - analysis |
| title | Antibody Binding to Fas Ligand Attenuates Inflammatory Cell Infiltration and Cytokine Secretion, Leading to Reduction of Myocardial Infarct Areas and Reperfusion Injury |
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