| Project/Area Number |
14570169
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | Nihon University |
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Principal Investigator |
YAMADA Tsutomu Nihon University, School of Medicine, Pathology, Assistant Prof, 医学部, 講師 (40182539)
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| Co-Investigator(Kenkyū-buntansha) |
OINUMA Toshinori Nihon University, School of Medicine, Pathology, Assistant Prof, 医学部, 講師 (30223704)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2003: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | PPARα / PPARγ / atherosclerosis / regression / depressed plaque / aorta / RT-PCR / foam cell |
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| Research Abstract |
To clarify relationships between the expression of PPARs and regression, we studied mRNA expression of PPARs subtypes with RTPCR, especially in centrally depressed atherosclerotic plaques (depressed plaque) in the aortas. Samples were separated from the depressed plaque, atheromatous plaque, and diffuse intimal thickening (DIT) at autopsy and they were analyzed for RT-PCR. The depressed plaques were divided into depressed area and surrounding elevated area. Total RNA was prepared, using the TRIzol Reagent, and was reverse transcribed using random hexamer primers and Thermoscript kit. Immunohistochemical analysis was processed for mouse anti-PPARγ antibody by the ABC method. 1) Foam cells in the depressed area were decreased than in the surrounding area of the depressed plaque. Strong reactivities for PPAR y were found in the nuclei of foam cells with immunostaining. 2) Expressions of PPARs mRNA were found both in the depressed area and the surrounding area. 3) PPARγ mRNA expression both in the depressed and the surrounding area, was greater than in DIT, and was less than in the atheromatous plaque. 4) Expression of PPARγ mRNA was increased in the surrounding area than in the depressed area. 5) A significant increase of PPARγ expression was found in the atheromatous plaque than in DIT. 6) There was no significant difference of PPAR a mRNA expression between the depressed area and the surrounding area. The depressed plaque has been proposed as a characteristic of regression in the recent studies. Expression of PPARs mRNA was detected in the depressed plaque as well as the atheromatous plaque, furthermore, there were different expressions and intensity of PPARs between the depressed area and the surrounding area of the depressed plaque. These findings suggest that the expression of PPARs may be involved not only in the progression of atherosclerosis but also in regression.
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