Source:http://linkedlifedata.com/resource/pubmed/id/10325241
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
|
pubmed:dateCreated |
1999-6-3
|
pubmed:abstractText |
Cross talk between oxidized LDL (ox-LDL) and angiotensin II (Ang II) may be relevant in atherosclerosis. In this study, we examined the presence of a specific endothelial receptor for ox-LDL (LOX-1) and Ang II receptors in human coronary artery endothelial cells (HCAECs). In addition, we studied the effect of Ang II on LOX-1 gene and protein expression. LOX-1 was consistently identified in HCAECs by reverse transcriptase-polymerase chain reaction (RT-PCR), cDNA sequence, Western blot, and 125I-labeled ox-LDL binding assay (Bmax, 29.7 ng/mg protein). The HCAECs also exhibited Ang II receptors (AT1>AT2), as determined by RT-PCR and 125I-labeled Ang II binding assay (Bmax, 2.21 and 1.19 fmol/mg protein, respectively). Incubation of HCAECs with Ang II markedly increased LOX-1 mRNA (RT-PCR) and protein (Western blot) expression. The increase in LOX-1 expression was dependent on Ang II concentration (10(-12) to 10(-6) mol/L). Ang II caused a concentration-dependent increase in 125I-labeled ox-LDL uptake by HCAECs and enhanced ox-LDL-mediated cell injury, as evident from an increase in LDH release and a decrease in cell viability. These effects of Ang II were completely blocked by pretreatment of HCAECs with losartan, a specific AT1 blocker, but not by PD123319, a specific AT2 blocker. These observations indicate the following: (1) HCAECs possess abundant LOX-1 as well as Ang II (AT1>AT2) receptors, (2) Ang II upregulates LOX-1 receptor and ox-LDL uptake, (3) the effects of Ang II are mediated by AT1 activation, and (4) Ang II enhances ox-LDL-mediated injury to HCAECs.
|
pubmed:commentsCorrections | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Culture Media,
http://linkedlifedata.com/resource/pubmed/chemical/L-Lactate Dehydrogenase,
http://linkedlifedata.com/resource/pubmed/chemical/Lipoproteins, LDL,
http://linkedlifedata.com/resource/pubmed/chemical/OLR1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Angiotensin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, LDL,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Oxidized LDL,
http://linkedlifedata.com/resource/pubmed/chemical/Scavenger Receptors, Class E,
http://linkedlifedata.com/resource/pubmed/chemical/oxidized low density lipoprotein
|
pubmed:status |
MEDLINE
|
pubmed:month |
May
|
pubmed:issn |
0009-7330
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
14
|
pubmed:volume |
84
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
1043-9
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:10325241-Angiotensin II,
pubmed-meshheading:10325241-Arteries,
pubmed-meshheading:10325241-Cell Survival,
pubmed-meshheading:10325241-Cells, Cultured,
pubmed-meshheading:10325241-Coronary Vessels,
pubmed-meshheading:10325241-Culture Media,
pubmed-meshheading:10325241-Endothelium, Vascular,
pubmed-meshheading:10325241-Humans,
pubmed-meshheading:10325241-L-Lactate Dehydrogenase,
pubmed-meshheading:10325241-Lipoproteins, LDL,
pubmed-meshheading:10325241-Receptor, Angiotensin, Type 1,
pubmed-meshheading:10325241-Receptor, Angiotensin, Type 2,
pubmed-meshheading:10325241-Receptors, Angiotensin,
pubmed-meshheading:10325241-Receptors, LDL,
pubmed-meshheading:10325241-Receptors, Oxidized LDL,
pubmed-meshheading:10325241-Scavenger Receptors, Class E,
pubmed-meshheading:10325241-Up-Regulation
|
pubmed:year |
1999
|
pubmed:articleTitle |
Upregulation of endothelial receptor for oxidized low-density lipoprotein (LOX-1) in cultured human coronary artery endothelial cells by angiotensin II type 1 receptor activation.
|
pubmed:affiliation |
Departments of Medicine and Physiology, University of Florida and Veterans Affairs Medical Center, Gainesville, FL, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
|