| Project/Area Number |
09670754
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Grant-in aid for Scientitic Research (c) |
|---|
Principal Investigator |
IWAMOTO Sanju Showa Univ., Dept.Med., Reseach Assocciate, 医学部, 助手 (50176567)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
HAGIWARA Tamio Showa Univ., Dept.Med., Reseach Assocciate, 医学部, 助手 (50228392)
|
|---|
| Project Period (FY) |
1997 – 1998
|
| Project Status |
Completed (Fiscal Year 1998)
|
| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥2,900,000 (Direct Cost: ¥2,900,000)
|
|---|
| Keywords | degenerated LDL / Atherosclerosis / cytochrome c oxidase / NADH Ubiguinone oxidoreductose / ヒトマクロファージ様細胞株 / デファレンシャルディスプレー法 |
|---|
| Research Abstract |
To exploit a strategy for prevention of atheroscrelosis, we analyzed messenger RNA (mRNA) expressed after phogocytosis of degenerated low density lipoprotein (d-LDL) on a human macrophage/dendritic-like cell line ELD-1, a subline of MABS-1. MRNA eluted from ELD-1 cells 2 days after phogocytosis of d-LDL, bioparticles of Eshelisia Coli (E. Coli), and cider pollen particles, were sampled to subtract mRNA of control cells by the methods of PCR select cDNA subtraction methods. To compare differences among those phagocytosed materials in the expression of mRNA, complementary DNA (cDNA) obtained by reverse transcription polymerase chain reaction (RT-PCR) was subjected to polyacrylamide gel electophoresis (PAGE). Though no fine bind was observed in the cDNA from d-LDL stimulating cells, two genes, which was expressed in both of E. Coli and cider pollen, were lost in d-LDL stimulation. DNA sequences of these genes were homologous completely to the part of human cytochrome c oxidase and NADH ubiquinone oxidoreductase. We speculated the possibility that mitochondria dysfunction caused by lipid peroxide might prevent expression of these genes because these were encoded mitochondrial proteins. We determined several unknown genes in these experiments. We will plane further experiments to clarify functions of the gene products.
|
