Linked Life Data

19167353

Source:http://linkedlifedata.com/resource/pubmed/id/19167353

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2009-3-9
pubmed:abstractText
We investigated the effects of serum amyloid A (SAA) on the production of C-C chemokine motif ligand 2 (CCL2) and the mechanism underlying SAA action in human umbilical vein endothelial cells (HUVECs). Stimulation of HUVECs by SAA elicited CCL2 production in a concentration-dependent manner. SAA induced the activations of NF-kappaB and AP-1, which were essential for CCL2 production after SAA stimulation. HUVECs expressed formyl peptide receptor-like 1 (FPRL1), and short interfering RNA knockdown of FPRL1 nearly completely blocked SAA-induced CCL2 production in HUVECs. We suggest that SAA stimulates CCL2 production via FPRL1 and, thus, contributes to atherosclerosis.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
1090-2104
pubmed:author
pubmed:issnType
Electronic
pubmed:day
6
pubmed:volume
380
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
313-7
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
Activation of formyl peptide receptor like-1 by serum amyloid A induces CCL2 production in human umbilical vein endothelial cells.
pubmed:affiliation
Department of Biochemistry, College of Medicine, Dong-A University, 3-1 Dongdaesindong Seogu, Busan 602-714, Republic of Korea.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't