PMID- 20216085
OWN - NLM
STAT- MEDLINE
DCOM- 20100816
LR  - 20220317
IS  - 1473-5598 (Electronic)
IS  - 0263-6352 (Linking)
VI  - 28
IP  - 6
DP  - 2010 Jun
TI  - LOX-1 mediates vascular lipid retention under hypertensive state.
PG  - 1273-80
LID - 10.1097/HJH.0b013e32833835d4 [doi]
AB  - 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.
FAU - Nakano, Atushi
AU  - Nakano A
AD  - Department of Vascular Physiology, National Cardiovascular Center Research 
      Institute, Suita, Osaka, Japan.
FAU - Inoue, Nobutaka
AU  - Inoue N
FAU - Sato, Yuko
AU  - Sato Y
FAU - Nishimichi, Norihisa
AU  - Nishimichi N
FAU - Takikawa, Kenji
AU  - Takikawa K
FAU - Fujita, Yoshiko
AU  - Fujita Y
FAU - Kakino, Akemi
AU  - Kakino A
FAU - Otsui, Kazunori
AU  - Otsui K
FAU - Yamaguchi, Saburo
AU  - Yamaguchi S
FAU - Matsuda, Haruo
AU  - Matsuda H
FAU - Sawamura, Tatsuya
AU  - Sawamura T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - J Hypertens
JT  - Journal of hypertension
JID - 8306882
RN  - 0 (OLR1 protein, rat)
RN  - 0 (Scavenger Receptors, Class E)
SB  - IM
CIN - J Hypertens. 2010 Jun;28(6):1127-8. PMID: 20467265
MH  - Animals
MH  - Blood Vessels/*metabolism
MH  - Hypertension/*metabolism
MH  - Immunohistochemistry
MH  - In Vitro Techniques
MH  - *Lipid Metabolism
MH  - Male
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Scavenger Receptors, Class E/*physiology
EDAT- 2010/03/11 06:00
MHDA- 2010/08/17 06:00
CRDT- 2010/03/11 06:00
PHST- 2010/03/11 06:00 [entrez]
PHST- 2010/03/11 06:00 [pubmed]
PHST- 2010/08/17 06:00 [medline]
AID - 10.1097/HJH.0b013e32833835d4 [doi]
PST - ppublish
SO  - J Hypertens. 2010 Jun;28(6):1273-80. doi: 10.1097/HJH.0b013e32833835d4.