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Activation of extracellular signal regulated kinase 1/2 in human dermal microvascular endothelial cells stimulated by anti-endothelial cell antibodies in sera of patients with Behçet's disease

Authors
 Kwang Hoon Lee  ;  Heun Jung Cho  ;  Hong Suk Kim  ;  Won Jae Lee  ;  Sungnack Lee  ;  Dongsik Bang 
Citation
 JOURNAL OF DERMATOLOGICAL SCIENCE, Vol.30(1) : 63-72, 2002 
Journal Title
 JOURNAL OF DERMATOLOGICAL SCIENCE 
ISSN
 0923-1811 
Issue Date
2002
MeSH
Autoantibodies/pharmacology ; Behcet Syndrome/blood ; Behcet Syndrome/enzymology* ; Behcet Syndrome/genetics ; Endothelium, Vascular/enzymology* ; Enzyme Activation ; Gene Expression Regulation/immunology ; Humans ; Intercellular Adhesion Molecule-1/genetics ; Interleukin-1/genetics ; Microcirculation/physiology ; Mitogen-Activated Protein Kinase 1/metabolism* ; Mitogen-Activated Protein Kinase 3 ; Mitogen-Activated Protein Kinases/metabolism* ; RNA, Messenger/genetics ; Reference Values ; Skin/blood supply* ; Tumor Necrosis Factor-alpha/genetics
Keywords
Antibodies ; Endothelial cells ; Behçet's disease ; ICAM-1 ; ERK 1/2
Abstract
Anti-endothelial cell antibodies (AECA) have been detected in the sera of patients with Behçet's disease (BD). The isotype of AECA from BD is IgM recognizing 44 kDa antigen (IgM-AECA) of human dermal microvascular endothelial cells (HDMEC). After stimulation of HDMEC with AECA-positive sera from BD patients, the expression of intercellular cell adhesion molecule-1 (ICAM-1) on HDMEC increases significantly. Mitogen-activated protein kinase (MAPK) cascade is one of protein kinase families activated by a wide spectrum of extracellular stimuli. There are several subtypes, including extracellular signal regulated kinase (ERK)1/2, c-Jun NH2 terminal kinase (JNK), and p38 cascades, and they regulate various cellular processes such as cell growth, differentiation, and inflammation. We examined the involvement of MAPK as a signal transduction pathway in the IgM-AECA-induced ICAM-1 expression. We used enzyme-linked immunosorbent assay (ELISA) and fluorescence-activated cell sorting (FACS) for detecting the induction of ICAM-1 on HDMEC. We also examined the production of tumor necrosis factor α (TNFα) or interleukin-1α (IL-1α) by HDMEC after stimulation with IgM-AECA, and checked the involvement of MAPK by Western blot assay. IgM-AECA cocktail from 8 patients with BD induced expression of the ICAM-1 on HDMEC. Neither TNFα nor IL-1α was detected by ELISA, FACS or reverse transcriptase-polymerase chain reaction in activated HDMEC cultures. IgM-AECA cocktail activated ERK1/2 and showed peak activities at 5 min after the stimulation. Specific MAPK/ERK kinase inhibitor PD98059 inhibited IgM-AECA-induced ERK1/2 activities and ICAM-1 expression on HDMEC at a concentration of 60 μM. IgM-AECA can play a pathogenic role in induction of vasculitis and inflammatory lesions of BD by directly activating endothelial cells, not by production of TNFα or IL-1α from HDMEC. ERK1/2 are involved in expression of ICAM-1 on HDMEC stimulated with IgM-AECA.
Full Text
http://www.sciencedirect.com/science/article/pii/S0923181102000622
DOI
10.1016/S0923-1811(02)00062-2
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers
Yonsei Authors
Bang, Dong Sik(방동식)
Lee, Kwang Hoon(이광훈)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/143865
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