Severity dependent up-regulations of LOX-1 and MCP-1 in early sclerotic changes of common carotid arteries in spontaneously hypertensive rats.
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.
Hamakawa
Y
Y
Department of Neurology, Graduate School of Medicine and Dentistry, Okayama University, Japan.
Omori
N
N
Ouchida
M
M
Nagase
M
M
Sato
K
K
Nagano
I
I
Shoji
M
M
Fujita
T
T
Abe
K
K
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000378:metabolism*; D015415:Biomarkers / Q000378:metabolism; D001835:Body Weight / Q000502:physiology; D001921:Brain / Q000502:physiology; D017536:Carotid Artery, Common / Q000378:metabolism*; D018932:Chemokine CCL2 / Q000235:genetics / Q000378:metabolism*; D004032:Diet; D006973:Hypertension / Q000235:genetics / Q000473:pathology*; D007150:Immunohistochemistry / Q000379:methods; D008055:Lipids / Q000097:blood; D008297:Male; D008955:Models, Cardiovascular; D009929:Organ Size; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D011918:Rats, Inbred SHR; D011921:Rats, Inbred WKY; D011973:Receptors, LDL / Q000235:genetics / Q000378:metabolism*; D051131:Receptors, Oxidized LDL; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D051127:Scavenger Receptors, Class E; D013997:Time Factors; D015854:Up-Regulation
D015415:Biomarkers; C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D008055:Lipids; C495136:OLR1 protein, rat; D012333:RNA, Messenger; D011973:Receptors, LDL; D051131:Receptors, Oxidized LDL; D051127:Scavenger Receptors, Class E