Protection of pancreatic islets by controlling both the volume-sensitive chloride channel and endoplasmic reticulum stress response
| Project/Area Number |
25861208
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Digestive surgery
|
|---|
| Research Institution | Fukushima Medical University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2013-04-01 – 2015-03-31
|
| Project Status |
Completed (Fiscal Year 2014)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 移植・再生医療 / 糖尿病 / 外科 / 膵島移植 / 外科学 / 小胞体ストレス |
|---|
| Outline of Final Research Achievements |
The purpose of this study is to protect pancreatic islets during isolation/transplantation procedures by controlling both the volume-sensitive chloride channel and endoplasmic reticulum (ER) stress response. Our results indicated that inhibition of Cl- influx into the cells reduced the cell damage during pancreas digestion, however, inhibition of Cl- influx did not reduce the damage during islet culture.
Whereas the ER stress responses had not changed in our experiment, IL1β and TNF were identified as the top upstream regulators during islet isolation and culture by analyzing microarray data. Regulating inflammatory response induced by inflammatory cytokines in isolated/cultured islets might be necessary to improve the efficacy of islet transplantation.
|
Report
(3 results)
Research Products
(12 results)
