| Project/Area Number |
26670429
|
|---|
| Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Kidney internal medicine
|
|---|
| Research Institution | Niigata University |
|---|
Principal Investigator |
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
後藤 眞 新潟大学, 医歯学系, 准教授 (00463969)
金子 佳賢 新潟大学, 医歯学系, 講師 (80444157)
|
|---|
| Research Collaborator |
SATO Yuya
|
|---|
| Project Period (FY) |
2014-04-01 – 2017-03-31
|
| Project Status |
Completed (Fiscal Year 2016)
|
| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
|
|---|
| Keywords | ネフローゼ症候群 / iPS細胞 / 糸球体上皮細胞 / プロラクチン / 性差 / 遺伝性ネフローゼ症候群 / Tリンパ球 / T細胞 / 初期化遺伝子 / FSGS / MCNS |
|---|
| Outline of Final Research Achievements |
The purpose of this study was to establish iPS cells from peripheral T-cells of healthy volunteers or patients with hereditary nephrotic syndrome, and to introduce differentiation into glomerular podocyte，and investigate their functions. We succeeded to establish the iPS cells and found that the differentiated cells from these iPSs were positive with nephrin, podocin, synaptopodin, podocalyxin. However, any functional difference was not observed on cells originated from patients with hereditary nephrotic syndrome as compared to those from healthy controls, in respect with the response to renin-angiotensin, inflammatory cytokines, etc. In parallel, we also demonstrated that male-predominant Mups expression and MUPs production and urine excretion were down-regulated, whereas female-predominant genes such as Cyp3a41 and Cyp3a44 expressions were up-regulated by prolactin, and that the regulatory role of prolactin was independent with sex-specific GH secretion pattern or testosterone.
|
