PMID- 15494120
OWN - NLM
STAT- MEDLINE
DCOM- 20050131
LR  - 20220408
IS  - 0161-6412 (Print)
IS  - 0161-6412 (Linking)
VI  - 26
IP  - 7
DP  - 2004 Oct
TI  - Severity dependent up-regulations of LOX-1 and MCP-1 in early sclerotic changes 
      of common carotid arteries in spontaneously hypertensive rats.
PG  - 767-73
AB  - Lectin-like oxidized low-density lipoprotein receptor (LOX-1) and monocyte 
      chemoattractant protein-1 (MCP-1) are molecules involving in the initiation and 
      progression of atherosclerosis. In order to examine a possible difference in 
      LOX-1 and MCP-1 expressions depending on the severity of early stage of 
      atherosclerosis, we investigated atherosclerotic changes by exposure to 
      hypertension and hyperlipidemia in common carotid arteries (CCAs) of stroke-prone 
      spontaneously hypertensive rat (SHR-SP). Three rat model groups such as control 
      [Wistar Kyoto rat (WKY) group], hypertension (SHR-SP group) and hypertension + 
      hyperlipidemia [SHR-SP + high fat and cholesterol (HFC) group] were used. Body 
      weights, brain weights, systolic blood pressures and serum levels of total 
      cholesterol, low-density lipoprotein and triglyceride were measured at 0, 5, 10 
      and 15 days after appropriate diet. Immunohistochemistry showed that the positive 
      area and the strength of LOX-1 and MCP-1 were larger in the SHR-SP + HFC group 
      than in the SHR-SP group, while no immunoreactivities were found in the WKY 
      group. Conventional RT-PCR and real-time PCR analyses showed that mRNAs of those 
      in the SHR-SP group were higher with greater up-regulation in the SHR-SP + HFC 
      group. LOX-1 and MCP-1 expressions were coordinately up-regulated at mRNA and 
      protein levels in an early stage of sclerosis depending on the severity of 
      atherosclerotic stress. Activations of LOX-1 and MCP-1 are collectively involved 
      in the early stage of atherosclerosis.
FAU - Hamakawa, Y
AU  - Hamakawa Y
AD  - Department of Neurology, Graduate School of Medicine and Dentistry, Okayama 
      University, Japan.
FAU - Omori, N
AU  - Omori N
FAU - Ouchida, M
AU  - Ouchida M
FAU - Nagase, M
AU  - Nagase M
FAU - Sato, K
AU  - Sato K
FAU - Nagano, I
AU  - Nagano I
FAU - Shoji, M
AU  - Shoji M
FAU - Fujita, T
AU  - Fujita T
FAU - Abe, K
AU  - Abe K
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Neurol Res
JT  - Neurological research
JID - 7905298
RN  - 0 (Biomarkers)
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipids)
RN  - 0 (OLR1 protein, rat)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, LDL)
RN  - 0 (Receptors, Oxidized LDL)
RN  - 0 (Scavenger Receptors, Class E)
SB  - IM
MH  - Animals
MH  - Arteriosclerosis/etiology/*metabolism
MH  - Biomarkers/metabolism
MH  - Body Weight/physiology
MH  - Brain/physiology
MH  - Carotid Artery, Common/*metabolism
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Diet
MH  - Hypertension/genetics/*pathology
MH  - Immunohistochemistry/methods
MH  - Lipids/blood
MH  - Male
MH  - Models, Cardiovascular
MH  - Organ Size
MH  - RNA, Messenger/biosynthesis
MH  - Rats
MH  - Rats, Inbred SHR
MH  - Rats, Inbred WKY
MH  - Receptors, LDL/genetics/*metabolism
MH  - Receptors, Oxidized LDL
MH  - Reverse Transcriptase Polymerase Chain Reaction/methods
MH  - Scavenger Receptors, Class E
MH  - Time Factors
MH  - Up-Regulation
EDAT- 2004/10/21 09:00
MHDA- 2005/02/03 09:00
CRDT- 2004/10/21 09:00
PHST- 2004/10/21 09:00 [pubmed]
PHST- 2005/02/03 09:00 [medline]
PHST- 2004/10/21 09:00 [entrez]
AID - 10.1179/016164104225016074 [doi]
PST - ppublish
SO  - Neurol Res. 2004 Oct;26(7):767-73. doi: 10.1179/016164104225016074.