THE ROLE OF PROTEIN-KINASE-C IN THE INDUCTION OF VCAM-1 EXPRESSION ON HUMAN UMBILICAL VEIN ENDOTHELIAL-CELLS

被引：60

作者：

DEISHER, TA ^{[1
]}

HADDIX, TL ^{[1
]}

MONTGOMERY, KF ^{[1
]}

POHLMAN, TH ^{[1
]}

KAUSHANSKY, K ^{[1
]}

HARLAN, JM ^{[1
]}

机构：

[1] UNIV WASHINGTON,DEPT SURG,SEATTLE,WA 98195

来源：

FEBS LETTERS | 1993年 / 331卷 / 03期

关键词：

PROTEIN KINASE-C; VASCULAR CELL ADHESION MOLECULE-1; TUMOR NECROSIS FACTOR-ALPHA; INTERLEUKIN-1-BETA; LIPOPOLYSACCHARIDE; HUMAN UMBILICAL VEIN ENDOTHELIAL CELL;

D O I：

10.1016/0014-5793(93)80354-W

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：

The role of protein kinase C (PKC) in interleukin-1beta-(Il-1beta)-, tumor necrosis factor-alpha- (TNF-alpha)-, and lipopolysaccharide- (LPS)-induced vascular cell adhesion molecule-1 (VCAM-1) expression on human umbilical vein endothelial cells (HUVEC) was studied. PKC inhibition or downregulation diminished VCAM-1 mRNA accumulation and protein expression. Interleukin-1beta, TNF-alpha, and LPS induce nuclear factor (NF)-kappaB-like binding activity, which precedes VCAM-1 transcription. PKC inhibition did not prevent NF-kappaB-like binding activity, indicating that this is PKC-independent, and NF-kappaB-like binding activity is insufficient for transcription of VCAM-1.

引用

收藏

页码：285 / 290

页数：6

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