title: Hypernuclear acetylation in atherosclerotic lesions and activated vascular smooth muscle cells.
abstract: Recent studies have implicated acetylation of several nuclear proteins such as histones and p53 on their epsilon-portion of lysine residues in eukaryotic transcription. Here we raised a specific polyclonal antibody against epsilon-acetylated lysine. Using the antibody, we detected hypernuclear acetylation (HNA) in atherosclerotic vascular smooth muscle cells (VSMCs). Thrombin, a humoral factor known to cause activation and proliferation of VSMCs, strongly potentiated HNA in cultured VSMCs. MAP kinase pathway and a signal coactivator CREB binding protein (CBP) were involved in thrombin-induced HNA of VSMCs. Our results suggest that coactivators cooperating with signal-dependent transcription activators play an important role in atherosclerogenesis via HNA in VSMCs.
authors.affiliation: Faculty of Medicine, Kagoshima University, 8-35-1 Sakuragaoka, Kagoshima, 890-8520, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Kawahara
authors.forename: S
authors.initials: S
authors.lastname: Watanabe
authors.forename: T
authors.initials: T
authors.lastname: Ohshima
authors.forename: Y
authors.initials: Y
authors.lastname: Soejima
authors.forename: T
authors.initials: T
authors.lastname: Oishi
authors.forename: S
authors.initials: S
authors.lastname: Aratani
authors.forename: M
authors.initials: M
authors.lastname: Nakata
authors.forename: M
authors.initials: M
authors.lastname: Shibata
authors.forename: K
authors.initials: K
authors.lastname: Inoue
authors.forename: T
authors.initials: T
authors.lastname: Amano
authors.forename: R
authors.initials: R
authors.lastname: Fujii
authors.forename: K
authors.initials: K
authors.lastname: Yanai
authors.forename: M
authors.initials: M
authors.lastname: Hagiwara
authors.forename: A
authors.initials: A
authors.lastname: Fukamizu
authors.forename: I
authors.initials: I
authors.lastname: Maruyama
authors.forename: T
authors.initials: T
authors.lastname: Nakajima
mesh_terms: D000107:Acetylation / Q000187:drug effects; D000906:Antibodies / Q000276:immunology; D002070:Butadienes / Q000494:pharmacology; D050882:CREB-Binding Protein; D002102:Cadaver; D002478:Cells, Cultured; D003324:Coronary Artery Disease / Q000378:metabolism*; D004789:Enzyme Activation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006388:Hemagglutinins / Q000378:metabolism; D006801:Humans; D007150:Immunohistochemistry; D008239:Lysine / Q000031:analogs & derivatives / Q000032:analysis / Q000276:immunology; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D009570:Nitriles / Q000494:pharmacology; D009687:Nuclear Proteins / Q000737:chemistry / Q000378:metabolism; D013917:Thrombin / Q000494:pharmacology; D015534:Trans-Activators / Q000378:metabolism; D014162:Transfection
chemical_list: D000906:Antibodies; D002070:Butadienes; D004791:Enzyme Inhibitors; D006388:Hemagglutinins; D009570:Nitriles; D009687:Nuclear Proteins; D015534:Trans-Activators; C113580:U 0126; C002315:N(alpha)-acetyllysine; C016949:N-epsilon-acetyllysine; D050882:CREB-Binding Protein; C494363:CREBBP protein, human; D020928:Mitogen-Activated Protein Kinases; D013917:Thrombin; D008239:Lysine