Phosphatidic acid에 의한 intercellular adhesion molecule-1 발현 조절에 관여하는 MAPK와 PKC-?의 역할
The role of mapk and pkc-?in phosphatidic acid-mediated intercellular adhesion molecule-1 expression
조우성, 윤홍식, 진병로, 백석환,
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조우성 ( Cho Woo-Sung ) - 영남대학교 의과대학 치과학교실
윤홍식 ( Yoon Hong-Sik ) - 영남대학교 의과대학 치과학교실
진병로 ( Chin Byung-Rho ) - 영남대학교 의과대학 치과학교실
백석환 ( Baek Suk-Hwan ) - 영남대학교 의과대학 생화학분자생물학교실
KMID : 0355620070330050445
Abstract
Background: Phosphatidic acid (PA), an important second messenger, is involved in inflammation. Notably, cell-cell interactions via adhesion molecules play a central role in inflammation. This thesis show that PA induces expression of intercellular adhesion molecule-1 (ICAM-1) on macrophages and describe the signaling pathways. MATERIALS AND
Methods:Macrophages were cultured in the presence of 10% FBS and assayed cell to cell adhesion using HUVEC. For the gene and protein analysis, RT-PCR, Western blot and flow cytometry were performed. In addition, overexpressed cell lines for dominant negative PKC-? mutant established and tested their effect on the promoter activity and expression of ICAM-1 protein by PA.
Results:PA-activated macrophages significantly increased adhering to human umbilical vein endothelial cell and this adhesion was mediated by ICAM-1. Pretreatment with rottlerin (PKC-?inhibitor) or expression of a dominant negative PKC-?mutant, but not Go6976 (classical PKC-? inhibitor) and myristoylated PKC-?inhibitor, attenuated PA-induced ICAM-1 expression. The p38 mitogen-activated protein kinase (MAPK) inhibitor blocked PA-induced ICAM-1 expression in contrast, ERK upstream inhibitor didn’t block ICAM-1.
Conclusions: These data suggest that PA-induced ICAM-1 expression and cell-cell adhesion in macrophages requires PKC-?activation and that PKC-?activation is triggers to sequential activation of p38 MAPK
키워드
Macrophage;ICAM-1;Adhesion;MAPK;Protein kinase C
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