DNA microarray analysis of gene expression in endothelial cells in response to 24-h shear stress

被引:213
作者
Chen, BPC
Li, YS
Zhao, YH
Chen, KD
Li, S
Lao, JM
Yuan, SL
Shyy, JYJ
Chien, S
机构
[1] Univ Calif San Diego, Dept Bioengn, La Jolla, CA 92093 USA
[2] Univ Calif San Diego, Whitaker Inst Biomed Engn, La Jolla, CA 92093 USA
[3] Univ Calif Riverside, Div Biomed Sci, Riverside, CA 92521 USA
关键词
DNA microarray; endothelial cells; gene expression; shear stress;
D O I
10.1152/physiolgenomics.2001.7.1.55
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The recently developed DNA microarray technology provides a powerful and efficient tool to rapidly compare the differential expression of a large number of genes. Using the DNA microarray approach, we investigated gene expression profiles in cultured human aortic endothelial cells (HAECs) in response to 24 h of laminar shear stress at 12 dyn/cm(2). This relatively long-term shearing of cultured HAECs led to the modulation of the expression of a number of genes. Several genes related to inflammation and EC proliferation were downregulated, suggesting that 24-h shearing may keep ECs in a relatively noninflammatory and nonproliferative state compared with static cells. Some genes were significantly upregulated by the 24-h shear stress; these includes genes involved in EC survival and angiogenesis (Tie2 and Flk-1) and vascular remodeling (matrix metalloproteinase 1). These results provide information on the profile of gene expression in shear-adapted ECs, which is the case for the native ECs in the straight part of the aorta in vivo.
引用
收藏
页码:55 / 63
页数:9
相关论文
共 55 条
[11]   THE DYNAMIC-RESPONSE OF VASCULAR ENDOTHELIAL-CELLS TO FLUID SHEAR-STRESS [J].
DEWEY, CF ;
BUSSOLARI, SR ;
GIMBRONE, MA ;
DAVIES, PF .
JOURNAL OF BIOMECHANICAL ENGINEERING-TRANSACTIONS OF THE ASME, 1981, 103 (03) :177-185
[12]   Shear stress inhibits apoptosis of human endothelial cells [J].
Dimmeler, S ;
Haendeler, J ;
Rippmann, V ;
Nehls, M ;
Zeiher, AM .
FEBS LETTERS, 1996, 399 (1-2) :71-74
[13]   Suppression of apoptosis by nitric oxide via inhibition of interleukin-1 beta-converting enzyme (ICE)-like and cysteine protease protein (CPP)-32-like proteases [J].
Dimmeler, S ;
Haendeler, J ;
Nehls, M ;
Zeiher, AM .
JOURNAL OF EXPERIMENTAL MEDICINE, 1997, 185 (04) :601-607
[14]   Downstream signalling events regulated by phosphatidylinositol 3-kinase activity [J].
Duronio, V ;
Scheid, MP ;
Ettinger, S .
CELLULAR SIGNALLING, 1998, 10 (04) :233-239
[15]   Blood vessel formation: What is its molecular basis? [J].
Folkman, J ;
DAmore, PA .
CELL, 1996, 87 (07) :1153-1155
[16]   FLOW EFFECTS ON PROSTACYCLIN PRODUCTION BY CULTURED HUMAN-ENDOTHELIAL CELLS [J].
FRANGOS, JA ;
ESKIN, SG ;
MCINTIRE, LV ;
IVES, CL .
SCIENCE, 1985, 227 (4693) :1477-1479
[17]  
Fukui Y, 1998, J BIOCHEM-TOKYO, V124, P1
[18]   Biomechanical activation of vascular endothelium as a determinant of its functional phenotype [J].
García-Cardeña, G ;
Comander, J ;
Anderson, KR ;
Blackman, BR ;
Gimbrone, MA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (08) :4478-4485
[19]   Vascular endothelial growth factor regulates endothelial cell survival through the phosphatidylinositol 3′-kinase Akt signal transduction pathway -: Requirement for Flk-1/KDR activation [J].
Gerber, HP ;
McMurtrey, A ;
Kowalski, J ;
Yan, MH ;
Keyt, BA ;
Dixit, V ;
Ferrara, N .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (46) :30336-30343
[20]   Hemodynamics, endothelial gene expression, and atherogenesis [J].
Gimbrone, MA ;
Resnick, N ;
Nagel, T ;
Khachigian, LM ;
Collins, T ;
Topper, JN .
ATHEROSCLEROSIS IV: RECENT ADVANCES IN ATHEROSCLEROSIS RESEARCH: THE FOURTH SARATOGA INTERNATIONAL CONFERENCE ON ATHEROSCLEROSIS, 1997, 811 :1-11