Document Detail

LOX-1 mediates vascular lipid retention under hypertensive state.
MedLine Citation:
PMID:  20216085     Owner:  NLM     Status:  MEDLINE    
OBJECTIVES: Hypertension is a powerful independent risk factor for atherosclerotic cardiovascular diseases; however, the precise molecular mechanisms whereby hypertension promotes atherosclerotic formation remain to be determined. The interaction between oxidized low-density lipoprotein (oxLDL) and its receptor lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) plays a critical role in atherogenesis. To clarify how hypertension promotes atherosclerosis, we investigated specific roles of LOX-1 in acceleration of lipid deposition under a hypertensive state. METHODS: We employed a model of stroke-prone spontaneously hypertensive rats (SHR-SP) that exhibits acute lipid deposition in mesenteric artery induced by high fat and salt loading. These vascular lipid deposition lesions share similar characteristics with the initial lesions of human atherosclerosis. RESULTS: The enhanced LOX-1 expression in SHR-SP was associated with oxidized LDL deposited in vascular wall. Anti-LOX-1 neutralizing antibody dramatically suppressed the lipid deposition in vivo in SHR-SP. Vitamin E decreased serum oxLDL-like LOX-1 ligands, and suppressed the vascular lipid deposition. The vascular permeability, evaluated by the leakage of Evans blue, was markedly enhanced by pretreatment of oxLDL. The enhancement of vascular permeability induced by oxLDL was suppressed by anti-LOX-1 antibody. CONCLUSION: The enhanced expression and activation of LOX-1 mediated the enhancement of vascular permeability, which contributed to the vascular lipid accumulation under hypertensive states.
Atushi Nakano; Nobutaka Inoue; Yuko Sato; Norihisa Nishimichi; Kenji Takikawa; Yoshiko Fujita; Akemi Kakino; Kazunori Otsui; Saburo Yamaguchi; Haruo Matsuda; Tatsuya Sawamura
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of hypertension     Volume:  28     ISSN:  1473-5598     ISO Abbreviation:  J. Hypertens.     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-14     Completed Date:  2010-08-16     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8306882     Medline TA:  J Hypertens     Country:  England    
Other Details:
Languages:  eng     Pagination:  1273-80     Citation Subset:  IM    
Department of Vascular Physiology, National Cardiovascular Center Research Institute, Suita, Osaka, Japan.
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MeSH Terms
Blood Vessels / metabolism*
Hypertension / metabolism*
Lipid Metabolism*
Rats, Inbred SHR
Rats, Inbred WKY
Reverse Transcriptase Polymerase Chain Reaction
Scavenger Receptors, Class E / physiology*
Reg. No./Substance:
0/Oldlr1 protein, rat; 0/Scavenger Receptors, Class E
Comment In:
J Hypertens. 2010 Jun;28(6):1127-8   [PMID:  20467265 ]

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