title: Phenotypic modulation of smooth muscle cells in human cerebral aneurysmal walls.
abstract: We used immunohistochemical methods to analyze the phenotypes of smooth muscle cells (SMCs) in human cerebral arteries and aneurysmal walls. Thirty-two aneurysmal walls were studied; 31 aneurysmal walls were resected at operation and 1 aneurysm was obtained at autopsy. Seven control arteries were obtained at autopsy. Semiserial sections were subjected to immunohistochemical staining with antibodies to alpha-smooth muscle actin (alpha-SMA), desmin and smooth muscle myosin heavy chain isoforms: SM1, SM2 and SMemb. In control cerebral arteries, SMCs in the media were strongly immunostained for alpha-SMA, desmin, SM1 and SM2; immunoreactivity for SMemb was faint or weakly positive. SMCs in both non-ruptured and ruptured aneurysmal walls showed no staining for desmin; the expression of alpha-SMA was well preserved. Compared with control cerebral arteries, in 4 of 11 non-ruptured aneurysmal walls, the staining intensity of SMCs for SMemb was clearly increased. In ruptured aneurysmal walls, the expression of SM2 was lower than in control cerebral arteries and non-ruptured aneurysmal walls. Our study suggests that the phenotype of SMCs in aneurysmal walls is different from the contractile type in the media of normal cerebral arteries, at least partially changing to the synthetic type in some non-ruptured aneurysms. SMCs in ruptured aneurysmal walls may have lost both phenotypes before rupture. Phenotypic modulation of SMCs in the aneurysmal walls appears to be related to a remodeling of the aneurysmal wall and to a rupture mechanism.
authors.affiliation: Department of Neurological Surgery, School of Medicine, The University of Tokushima, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Nakajima
authors.forename: S
authors.initials: S
authors.lastname: Nagahiro
authors.forename: T
authors.initials: T
authors.lastname: Sano
authors.forename: J
authors.initials: J
authors.lastname: Satomi
authors.forename: K
authors.initials: K
authors.lastname: Satoh
mesh_terms: D000199:Actins / Q000378:metabolism; D000328:Adult; D000368:Aged; D017542:Aneurysm, Ruptured / Q000378:metabolism / Q000473:pathology; D003893:Desmin / Q000378:metabolism; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D002532:Intracranial Aneurysm / Q000378:metabolism / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology*; D018995:Myosin Heavy Chains / Q000378:metabolism; D010641:Phenotype
chemical_list: D000199:Actins; D003893:Desmin; D018995:Myosin Heavy Chains