PMID- 11937582
OWN - NLM
STAT- MEDLINE
DCOM- 20020523
LR  - 20190515
IS  - 0022-1767 (Print)
IS  - 0022-1767 (Linking)
VI  - 168
IP  - 8
DP  - 2002 Apr 15
TI  - Antiphospholipid antibodies induce monocyte chemoattractant protein-1 in 
      endothelial cells.
PG  - 4209-15
AB  - The presence of antiphospholipid Ab is associated with increased risk of 
      thrombosis. The monocyte-endothelial cell interaction has been suggested to play 
      a key role at the site of vascular injury during thrombosis. Therefore, we tested 
      the effect of anticardiolipin Abs (aCL) on the production of monocyte 
      chemoattractant protein-1 (MCP-1) in HUVEC. We found that monoclonal aCL as well 
      as IgG fractions from patients with antiphospholipid syndrome (APS-IgG) could 
      induce the production of MCP-1 in HUVEC. The ability of IgG aCL to induce MCP-1 
      production could be abrogated by preabsorption with cardiolipin liposomes. 
      Simultaneous addition of either monoclonal aCL or APS-IgG with IL-1beta resulted 
      in synergistic increase in MCP-1 production, whereas the addition of control IgG 
      lacking aCL activity did not alter IL-1beta-induced levels of MCP-1. MCP-1 mRNA 
      expression was also up-regulated when HUVEC were incubated with either APS-IgG or 
      monoclonal aCL, and down-regulated by the treatment of dexamethasone. In 
      addition, we found that serum levels of MCP-1 in 76 systemic lupus erythematosus 
      patients correlated well with the titers of IgG aCL. Collectively, these results 
      indicate that aCL could promote endothelial cell-monocyte cross-talk by enhancing 
      the endothelial production of MCP-1, thereby shifting the hemostatic balance 
      toward the prothrombotic state of APS.
FAU - Cho, Chul-Soo
AU  - Cho CS
AD  - Department of Medicine, Division of Rheumatology, Center for Rheumatic Diseases, 
      Kangnam St. Mary's Hospital, Catholic University of Korea, Seoul, Korea. 
      chocs@cmc.cuk.ac.kr
FAU - Cho, Mi-La
AU  - Cho ML
FAU - Chen, Pojen P
AU  - Chen PP
FAU - Min, So-Youn
AU  - Min SY
FAU - Hwang, Sue-Yun
AU  - Hwang SY
FAU - Park, Kyung-Soo
AU  - Park KS
FAU - Kim, Wan-Uk
AU  - Kim WU
FAU - Min, Do-June
AU  - Min DJ
FAU - Min, Jun-Ki
AU  - Min JK
FAU - Park, Sung-Hwan
AU  - Park SH
FAU - Kim, Ho-Youn
AU  - Kim HY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Immunol
JT  - Journal of immunology (Baltimore, Md. : 1950)
JID - 2985117R
RN  - 0 (Adjuvants, Immunologic)
RN  - 0 (Antibodies, Anticardiolipin)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Glycoproteins)
RN  - 0 (Immunoglobulin G)
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Interleukin-1)
RN  - 0 (RNA, Messenger)
RN  - 0 (beta 2-Glycoprotein I)
RN  - 7S5I7G3JQL (Dexamethasone)
SB  - IM
MH  - Adjuvants, Immunologic/pharmacology
MH  - Adult
MH  - Antibodies, Anticardiolipin/blood/*pharmacology
MH  - Cells, Cultured
MH  - Chemokine CCL2/antagonists & inhibitors/*biosynthesis/blood/genetics
MH  - Dexamethasone/pharmacology
MH  - Drug Synergism
MH  - Endothelium, Vascular/cytology/*immunology/*metabolism
MH  - Female
MH  - Glycoproteins/physiology
MH  - Humans
MH  - Immunoglobulin G/blood
MH  - Immunosuppressive Agents/pharmacology
MH  - Interleukin-1/pharmacology
MH  - Lupus Erythematosus, Systemic/blood/immunology
MH  - Male
MH  - RNA, Messenger/biosynthesis
MH  - beta 2-Glycoprotein I
EDAT- 2002/04/09 10:00
MHDA- 2002/05/25 10:01
CRDT- 2002/04/09 10:00
PHST- 2002/04/09 10:00 [pubmed]
PHST- 2002/05/25 10:01 [medline]
PHST- 2002/04/09 10:00 [entrez]
AID - 10.4049/jimmunol.168.8.4209 [doi]
PST - ppublish
SO  - J Immunol. 2002 Apr 15;168(8):4209-15. doi: 10.4049/jimmunol.168.8.4209.