PMID- 15136050
OWN - NLM
STAT- MEDLINE
DCOM- 20040913
LR  - 20131121
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 174
IP  - 2
DP  - 2004 Jun
TI  - Aspirin inhibits monocyte chemoattractant protein-1 and interleukin-8 expression 
      in TNF-alpha stimulated human umbilical vein endothelial cells.
PG  - 207-13
AB  - Atherosclerosis and its complications such as stroke, myocardial infraction and 
      peripheral vascular disease, remain the major causes of morbidity and mortality 
      in the world. Studies have showed that chemokines and adhesion molecules are 
      involved in causing atherosclerosis by promoting directed migration of 
      inflammatory cells. Monocyte chemoattractant protein-1 (MCP-1) is one of the key 
      factors critical for the initiating and developing of atherosclerotic lesions. 
      IL-8, a CXC chemokine, stimulates neutrophil chemotaxis. Aspirin is the most 
      common drug used to prevent the complications of atherosclerosis such as stroke 
      and coronary heart disease. In this study, we found that aspirin inhibited 
      TNF-alpha (10 ng/ml)-induced MCP-1 and IL-8 expression at the RNA and protein 
      levels in human umbilical vein endothelial cells (HUVECs), monocyte adhesion and 
      transmigration, and that its inhibitory effects were not due to decreased HUVEC 
      viability as assessed by MTT test. Aspirin at the dose as low as 10 microg/ml 
      significantly inhibited the release of TNF-stimulated MCP-1 by 29.1% (P = 0.008) 
      and IL-8 by 26.9% (P = 0.0146) as compared to TNF-stimulated release. Antibodies 
      pretreatment were likely to decrease the production of MCP-1 (P < 0.0001) and 
      IL-8 (P < 0.0001). Furthermore, aspirin (10 microg/ml) inhibited U937 cell 
      adhesion by a 13.4% (P = 0.0119) inhibition as compared to TNF-stimulated alone. 
      Finally, at higher concentration, aspirin also inhibited U937 migration to HUVEC 
      by 89.1% (P = 0.0475) as compared to TNF-stimulated alone. These results in our 
      study suggest that aspirin inhibits TNF-alpha stimulated MCP-1 and IL-8 release 
      in HUVECs, for its additional therapeutic effects of aspirin in causing 
      atherosclerosis.
FAU - Yang, Yi-Yuan
AU  - Yang YY
AD  - Department of Neurology, Jen-Ai Hospital, Taipei, Taiwan, ROC.
FAU - Hu, Chaur-Jong
AU  - Hu CJ
FAU - Chang, Su-Mei
AU  - Chang SM
FAU - Tai, Tzu-Yi
AU  - Tai TY
FAU - Leu, Sy-Jye
AU  - Leu SJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-8)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - R16CO5Y76E (Aspirin)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/prevention & control
MH  - Aspirin/*pharmacology
MH  - Cell Adhesion/drug effects
MH  - Cell Movement/physiology
MH  - Cells, Cultured
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Endothelial Cells/*drug effects/metabolism
MH  - Humans
MH  - Interleukin-8/genetics/*metabolism
MH  - Probability
MH  - RNA, Messenger/analysis
MH  - Reverse Transcriptase Polymerase Chain Reaction/methods
MH  - Sensitivity and Specificity
MH  - Tumor Necrosis Factor-alpha/*antagonists & inhibitors
MH  - Umbilical Veins/cytology
EDAT- 2004/05/12 05:00
MHDA- 2004/09/14 05:00
CRDT- 2004/05/12 05:00
PHST- 2003/08/14 00:00 [received]
PHST- 2004/01/12 00:00 [revised]
PHST- 2004/01/22 00:00 [accepted]
PHST- 2004/05/12 05:00 [pubmed]
PHST- 2004/09/14 05:00 [medline]
PHST- 2004/05/12 05:00 [entrez]
AID - S0021-9150(04)00084-X [pii]
AID - 10.1016/j.atherosclerosis.2004.01.024 [doi]
PST - ppublish
SO  - Atherosclerosis. 2004 Jun;174(2):207-13. doi: 
      10.1016/j.atherosclerosis.2004.01.024.