title: Neutrophil accumulation promotes intimal hyperplasia after photochemically induced arterial injury in mice.
abstract: The role of leukocytes in the pathogenesis of coronary arterial disease has become a focus for clinical research. The aim of this study was to determine whether neutrophil accumulation would participate in the development of intimal hyperplasia after endothelial injury in mice, and whether d-myo-inositol hexakisphosphate (phytic acid) which inhibits the binding of L- and P-selectin to sialyl Lewis(X) could inhibit the development of intimal hyperplasia. Endothelial injury was inflicted in one femoral artery via the photochemical reaction between systemically injected rose bengal and transillumination with green light (wavelength: 540 nm). Scanning electron microscopic observation at 3 days after the injury showed an increase in the number of leukocytes adhering to the injury site. Histological observation at 21 days showed that in the neutropenia group administered anti-neutrophil antibody and in the phytic acid-treated group the progression of intimal hyperplasia was significantly attenuated by comparison with the corresponding control groups. These results suggest that neutrophil accumulation contributes to the initiation and/or development of intimal hyperplasia and L- and/or P-selectin may participate in their mechanisms.
authors.affiliation: Department of Pharmacology, Hamamatsu University School of Medicine, 3600, Handa-cho, Hamamatsu 431-3124, Japan. shimazawa@gifu-pu.ac.jp
authors.forename: Masamitsu
authors.initials: M
authors.lastname: Shimazawa
authors.forename: Shinji
authors.initials: S
authors.lastname: Watanabe
authors.forename: Kazunao
authors.initials: K
authors.lastname: Kondo
authors.forename: Hideaki
authors.initials: H
authors.lastname: Hara
authors.forename: Mitsuyoshi
authors.initials: M
authors.lastname: Nakashima
authors.forename: Kazuo
authors.initials: K
authors.lastname: Umemura
mesh_terms: D000818:Animals; D000906:Antibodies / Q000008:administration & dosage / Q000494:pharmacology; D002448:Cell Adhesion / Q000276:immunology; D002478:Cells, Cultured; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000276:immunology* / Q000473:pathology; D005263:Femoral Artery; D006801:Humans; D006965:Hyperplasia / Q000276:immunology; D008027:Light; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D032389:Myocytes, Smooth Muscle / Q000187:drug effects; D009503:Neutropenia / Q000139:chemically induced / Q000276:immunology; D009504:Neutrophils / Q000276:immunology / Q000473:pathology; D016491:Peripheral Vascular Diseases / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D010538:Peritonitis / Q000139:chemically induced / Q000517:prevention & control; D010833:Phytic Acid / Q000008:administration & dosage / Q000494:pharmacology; D010973:Platelet Adhesiveness; D012395:Rose Bengal; D013864:Thioglycolates; D017539:Tunica Intima / Q000187:drug effects / Q000276:immunology* / Q000473:pathology
chemical_list: D000906:Antibodies; D013864:Thioglycolates; D012395:Rose Bengal; D010833:Phytic Acid