Proteasome-dependent decrease in Akt by growth factors in vascular smooth muscle cells

被引:37
作者
Adachi, M
Katsumura, KR
Fujii, K
Kobayashi, S
Aoki, H
Matsuzaki, M
机构
[1] Yamaguchi Univ, Sch Med, Dept Mol Cardiovasc Biol, Ube, Yamaguchi 7558505, Japan
[2] Yamaguchi Univ, Sch Med, Dept Mol Physiol, Ube, Yamaguchi 7558505, Japan
关键词
Akt; vascular smooth muscle cell; proteasome; ubiquitin; platelet-derived growth factor; insulin-like growth factor-1; phosphatidylinositol; 3-kinase;
D O I
10.1016/S0014-5793(03)01109-8
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Akt is activated by growth factors to regulate various aspects of vascular smooth muscle cell function. Platelet-derived growth factor (PDGF) and insulin-like growth factor-1 activated Akt in vascular smooth muscle cells with a rapid reduction of total Akt protein that lasted for several hours. The downregulation of Akt required phosphatidylinositol 3-kinase activity, but not intrinsic Akt activity. The downregulation of Akt was abrogated by MG-132, a proteasome inhibitor, but not by inhibitors of calpain or cathepsins. Akt was found in ubiquitin immune complex after PDGF treatment. Proteasome-dependent degradation of Akt may provide a counter-regulatory mechanism against overactivation of Akt. (C) 2003 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:77 / 80
页数:4
相关论文
共 25 条
[1]   Regulation of vascular smooth muscle cell apoptosis - Modulation of bad by a phosphatidylinositol 3-kinase-dependent pathway [J].
Bai, HZ ;
Pollman, MJ ;
Inishi, Y ;
Gibbons, GH .
CIRCULATION RESEARCH, 1999, 85 (03) :229-237
[2]   Akt forms an intracellular complex with heat shock protein 90 (Hsp90) and Cdc37 and is destabilized by inhibitors of Hsp90 function [J].
Basso, AD ;
Solit, DB ;
Chiosis, G ;
Giri, B ;
Tsichlis, P ;
Rosen, N .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (42) :39858-39866
[3]   The insulin-like growth factor axis - A review of atherosclerosis and restenosis [J].
Bayes-Genis, A ;
Conover, CA ;
Schwartz, RS .
CIRCULATION RESEARCH, 2000, 86 (02) :125-130
[4]   EXPRESSION OF A CONSTITUTIVE NF-KAPPA-B-LIKE ACTIVITY IS ESSENTIAL FOR PROLIFERATION OF CULTURED BOVINE VASCULAR SMOOTH-MUSCLE CELLS [J].
BELLAS, RE ;
LEE, JS ;
SONENSHEIN, GE .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 96 (05) :2521-2527
[5]   Phosphatidylinositol 3-kinase is required for insulin-like growth Factor-I-Induced vascular smooth muscle cell proliferation and migration [J].
Duan, C ;
Bauchat, JR ;
Hsieh, T .
CIRCULATION RESEARCH, 2000, 86 (01) :15-23
[6]   ROLE OF PLATELETS IN SMOOTH-MUSCLE CELL-PROLIFERATION AND MIGRATION AFTER VASCULAR INJURY IN RAT CAROTID-ARTERY [J].
FINGERLE, J ;
JOHNSON, R ;
CLOWES, AW ;
MAJESKY, MW ;
REIDY, MA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1989, 86 (21) :8412-8416
[7]   Growth factors and mitogen activated protein kinases [J].
Force, T ;
Bonventre, JV .
HYPERTENSION, 1998, 31 (01) :152-161
[8]   BCR/ABL regulates expression of the cyclin-dependent kinase inhibitor p27Kip1 through the phosphatidylinositol 3-kinase/AKT pathway [J].
Gesbert, F ;
Sellers, WR ;
Signoretti, S ;
Loda, M ;
Griffin, JD .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (50) :39223-39230
[9]   LOCALIZATION OF INSULIN-LIKE GROWTH-FACTOR-I AND INHIBITION OF CORONARY SMOOTH-MUSCLE CELL-GROWTH BY SOMATOSTATIN ANALOGS IN HUMAN CORONARY SMOOTH-MUSCLE CELLS - A POTENTIAL TREATMENT FOR RESTENOSIS [J].
GRANT, MB ;
WARGOVICH, TJ ;
ELLIS, EA ;
CABALLERO, S ;
MANSOUR, M ;
PEPINE, CJ .
CIRCULATION, 1994, 89 (04) :1511-1517
[10]   Differentiated phenotype of smooth muscle cells depends on signaling pathways through insulin-like growth factors and phosphatidylinositol 3-kinase [J].
Hayashi, K ;
Saga, H ;
Chimori, Y ;
Kimura, K ;
Yamanaka, Y ;
Sobue, K .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (44) :28860-28867