title: Possible involvement of myofibroblast in the development of inflammatory aortic aneurysm.
abstract: To clarify the role of myofibroblasts in the development of inflammatory aortic aneurysm (IAA), 11 cases of IAA (69.2+/-8.59 years) were investigated immunohistochemically and were morphometrically compared with 12 age-matched cases of atherosclerotic abdominal aneurysm (AAA, 69.6+/-5.94 years). The positivity of mantle sign and CRP was significantly higher in the IAA group than in the AAA group. The wall of IAA (5.41+/-1.47 mm) was significantly thicker than that of AAA (2.68+/-0.71 mm). A significant increase in the expression of alpha-smooth muscle actin was found in adventitial fibroblasts of IAA compared to those of AAA. The cell density and MIB-1 index of adventitial myofibroblasts were significantly higher in IAA than in AAA (cell density: 1.69+/-0.51 vs. 1.09+/-0.4 x 10(3) cells/mm(2); MIB-1 index: 5.25+/-2.97% vs. 1.55+/-0.71%). IAA showed a significantly lower area ratio (MAR) of adventitial microvessels than did AAA (2.92+/-1.49% vs. 7.51+/-2.64%). However, there was no significant difference in microvessel density (MVD) between IAA and AAA (84.62+/-50.5 vs. 65.1+/-32.6 vessels/mm(2)). In some cases of IAA, adventitial myofibroblasts expressed hypoxia-inducible factor 1alpha in their cytoplasm or nuclei while it was not detected in AAA. These findings suggest that the development of IAA may be partly mediated by the proliferation of adventitial myofibroblasts, which might be related to tissue hypoxia.
authors.affiliation: Department of Pathology, School of Medicine, Fukuoka University, 45-1, 7-chome Nanakuma, Jonan-ku, Fukuoka 814-0180, Japan. nysakata@fukuoka-u.ac.jp <nysakata@fukuoka-u.ac.jp>
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Sakata
authors.forename: Kazuki
authors.initials: K
authors.lastname: Nabeshima
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Iwasaki
authors.forename: Tadashi
authors.initials: T
authors.lastname: Tashiro
authors.forename: Noriko
authors.initials: N
authors.lastname: Uesugi
authors.forename: Osamu
authors.initials: O
authors.lastname: Nakashima
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Ito
authors.forename: Takemi
authors.initials: T
authors.lastname: Kawanami
authors.forename: Kiyomi
authors.initials: K
authors.lastname: Furuya
authors.forename: Masaru
authors.initials: M
authors.lastname: Kojima
mesh_terms: D000199:Actins / Q000378:metabolism; D000368:Aged; D000369:Aged, 80 and over; D000785:Aneurysm, Infected / Q000378:metabolism / Q000473:pathology*; D001012:Aorta, Abdominal / Q000378:metabolism / Q000473:pathology*; D017544:Aortic Aneurysm, Abdominal / Q000378:metabolism / Q000473:pathology*; D002452:Cell Count; D003238:Connective Tissue / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D005260:Female; D005347:Fibroblasts / Q000378:metabolism / Q000473:pathology*; D019084:Fluorescent Antibody Technique, Indirect; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000378:metabolism; D007124:Immunoenzyme Techniques; D019394:Ki-67 Antigen / Q000378:metabolism; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D032389:Myocytes, Smooth Muscle / Q000378:metabolism / Q000473:pathology*
chemical_list: D000199:Actins; C497442:HIF1A protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D019394:Ki-67 Antigen