Vaspin Can Not Inhibit TNF-α-Induced Inflammation of Human Umbilical Vein Endothelial Cells

被引:22
作者
Fu, Ben-Dong [1 ,2 ]
Yamawaki, Hideyuki [1 ]
Okada, Muneyoshi [1 ]
Hara, Yukio [1 ]
机构
[1] Kitasato Univ, Sch Vet Med, Dept Vet Pharmacol, Towada, Aomori 0348628, Japan
[2] Jilin Univ, Coll Anim Sci & Vet Med, Dept Clin Vet Med, Changchun 130062, Jilin, Peoples R China
关键词
adipokine; endothelial cell; inflammation; signal transduction; NF-KAPPA-B; VISCERAL ADIPOSE-TISSUE; SERINE-PROTEASE INHIBITOR; VASCULAR INFLAMMATION; ADIPOKINE VASPIN; EXPRESSION; PATHWAY; OBESITY; KINASE; ADIPOCYTOKINE;
D O I
10.1292/jvms.71.1201
中图分类号
S85 [动物医学(兽医学)];
学科分类号
0906 ;
摘要
Visceral adipose tissue-derived serine protease inhibitor (vaspin) has been recently identified as an adipocytokine in a rat model of type 2 diabetes. Adipocytokines may directly influence the function of endothelial cells (ECs) and modulate inflammatory states. We therefore assessed the effects of vaspin on basal and TNF-alpha-stimulated human umbilical vein ECs. Vaspin (10-100 ng/ml, 24 hr) had no effects on both basal ECs morphology and TNF-alpha-induced (10 ng/ml, 24 hr) morphological damages. Vaspin did not inhibit the TNF-alpha (20 min) activation of JNK, p38 and NF-kappa B, but only slightly inhibited Akt. Furthermore, vaspin did not decrease the TNF-alpha (24 hr) induction of vascular cell adhesion molecule-1, intercellular adhesion molecule-1, endothelial selectin, and cyclooxygenase-2 protein expression as well as monocyte chemotactic protein-1, tissue factor, and plasmogen activator inhibitor-1 mRNA expression. The present results indicate that vaspin has no effects on normal ECs, and can not prevent TNF-alpha-induced inflammatory injury.
引用
收藏
页码:1201 / 1207
页数:7
相关论文
共 38 条
[31]  
WOZNIAK SE, DIG DIS SCI IN PRESS
[32]   Cytotoxicity of water-soluble fullerene in vascular endothelial cells [J].
Yamawaki, H ;
Iwai, N .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2006, 290 (06) :C1495-C1502
[33]   Fluid shear stress inhibits vascular inflammation by decreasing thioredoxin-interacting protein in endothelial cells [J].
Yamawaki, H ;
Pan, S ;
Lee, RT ;
Berk, BC .
JOURNAL OF CLINICAL INVESTIGATION, 2005, 115 (03) :733-738
[34]   Glyoxal causes inflammatory injury in human vascular endothelial cells [J].
Yamawaki, Hideyuki ;
Hara, Yukio .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2008, 369 (04) :1155-1159
[35]   Methylglyoxal mediates vascular inflammation via JNK and p38 in human endothelial cells [J].
Yamawaki, Hideyuki ;
Saito, Kazuaki ;
Okada, Muneyoshi ;
Hara, Yukio .
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY, 2008, 295 (06) :C1510-C1517
[36]   Serum vaspin concentrations in human obesity and type 2 diabetes [J].
You, Byung-Soo ;
Kloeting, Nora ;
Kratzsch, Juergen ;
Lee, Namseok ;
Park, Ji Woo ;
Song, Eun-Sun ;
Ruschke, Karen ;
Oberbach, Andreas ;
Fasshauer, Mathias ;
Stumvoll, Michael ;
Blueher, Matthias .
DIABETES, 2008, 57 (02) :372-377
[37]   TNFR1-induced NF-κB, but not ERK, p38MAPK or JNK activation, mediates TNF-induced ICAM-1 and VCAM-1 expression on endothelial cells [J].
Zhou, Zhigang ;
Connell, Michelle C. ;
MacEwan, David J. .
CELLULAR SIGNALLING, 2007, 19 (06) :1238-1248
[38]   Role of NF-κB and PI 3-kinase/Akt in TNF-α-induced cytotoxicity in microvascular endothelial cells [J].
Zhou, Zhu ;
Gengaro, Patricia ;
Wang, Wei ;
Wang, Xue-qing ;
Li, Chunling ;
Faubel, Sarah ;
Rivard, Christopher ;
Schrier, Robert W. .
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY, 2008, 295 (04) :F932-F941