| Project/Area Number |
09672345
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Laboratory medicine
|
|---|
| Research Institution | HOKKAIDO UNIVERSITY |
|---|
Principal Investigator |
MATSUNO Kazuhiko College of Medical Technology, Hokkaido Univ., Professor, 医療技術短期大学部, 教授 (70102332)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
CHIBA Hitoshi Medical hospital School of Med., Hokkaido Univ., Lec., 医学部・附属病院, 講師 (70197622)
|
|---|
| Project Period (FY) |
1997 – 1998
|
| Project Status |
Completed (Fiscal Year 1998)
|
| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1998: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1997: ¥2,100,000 (Direct Cost: ¥2,100,000)
|
|---|
| Keywords | platelets / CD36 / lipoprotein / LDL / oxidized-LDL / total cholesterol / CD62P / CD63 / カルシウム |
|---|
| Research Abstract |
Oxidized-low density lipoprotein (ox-LDL), but not native LDL (n-LDL), induced platelet aggregation in washed platelet suspension, and induced the expression of CD62P and CD63 on platelets. N-LDL and native high density lipoprotein (n-HDL) inhibited ox-LDL-induced platelet aggregation. Monoclonal antibody against CD36 inhibited low concentration of ox-LDL-induced potentiation of thrombin-induced platelet aggregation. Ox-LDL-induced CD62P and CD63 expression was inferior in CD36 negative subjects than in CD36 positive subjects. Taken together, ox-LDL-induced platelet activation was considered to be partly mediated by CD36 on platelets.
We screened CD36 antigen on platelets and monocytes using flow cytometry in 1094 Japanese healthy volunteers, and studied the phenotype-genotype relationship of CD36 deficiency. The type I CD36 deficiency (negative CD36 on both platelets and monocytes) and type II CD36 deficiency (negative CD36 on only platelets) were found in 9(0.82%) and 59(5.39%), respectively. Of the 56 with phenotypic CD36 deficiency, 34(61%) had one or two reported mutations. No reported mutation was detected in 22 with typeII deficiency. The substituion of T for C at nt 478 constituted the major cause of type I deficiency. Total cholesterol level and LDL-cholesterol level were higher in CD36 negative subjects than in CD36 positive subjects. It is considered that the relationship LDL (and/or ox-LDL) and platelets was changed in CD36 negative subjects.
|
