| Project/Area Number |
08457349
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Thoracic surgery
|
|---|
| Research Institution | Osaka University |
|---|
Principal Investigator |
SHIRAKURA Ryota Osaka University Medical School, Professor, 医学部, 教授 (00116047)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
FUKUSHIMA Norihide Osaka University Medical School, Assistant Professor, 医学部, 助手 (30263247)
SAWA Yoshiki Osaka University Medical School, Assistant Professor, 医学部, 助手 (00243220)
NAKATA Seizo Osaka University Medical School, Associate Professor, 医学部, 助教授 (50116068)
MIYAGAWA Shuji Osaka University Medical School, Assistant Professor, 医学部, 助手 (90273648)
|
|---|
| Project Period (FY) |
1996 – 1997
|
| Project Status |
Completed (Fiscal Year 1997)
|
| Budget Amount *help |
¥7,800,000 (Direct Cost: ¥7,800,000)
Fiscal Year 1997: ¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1996: ¥5,300,000 (Direct Cost: ¥5,300,000)
|
|---|
| Keywords | rat heart graft / retransplantation technique / Tranplant vasculopathy / PCR / ラット / SRY遺伝子 / In Situ PCR法 |
|---|
| Research Abstract |
To determine the origin of infiltrating cells in a retransplnted heart in our rat chronic rejection model, we have tried to establish the PCR in situ hybridization technique using a male specific gene, SRY,and a male dominant repetitive DNA sequence, RN91ES8, as targets. Despite the meticulous titration of fixation time, conditions of protease treatment, PCR conditions or the selection of ptimers and probes, it as not possible for us to detect a specific signal in the tissue. Then, we moved to the establishment of semi-quantitation of rat cytokine mRNA by RT-PCR techniques. We have now almost succeeded to quantitate about 40 different rat cytokine mRNAs expressed in transplanted heart. We are studying the molecular mechanisms underlying transplant vasculopathy in our rat heart-retransplantation model right now.
Trying to establish the molecular techniques on the one hand, we have studied the pathophysiology of the disease using conventional techniques on the other. The studies listed in the publication table revealed that the critical immune responses within the first 5 days after transplantation determined the occurrence of transplant vasculopathy and showed that either CD4+ or CD8+ T cells and macrophages were essential for the critical immune responses. Moreover, the experiments retransplantting an allograft into a F1 animal or a nude rat indicated that the alloimmune responses by T cells after the initial period from the transplantation are dispensable for the progression of the disease. We are applying the molecular techniques established in this study on this unique model of transplant vasculopathy to elucidate the molecular mechanisms of the disease.
|
