New strategy for drug development of cerebral ischemia; zinc signal is a potential target
| Project/Area Number |
23590644
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Applied pharmacology
|
|---|
| Research Institution | Gifu Pharmaceutical University |
|---|
Principal Investigator |
HARA Hirokazu 岐阜薬科大学, 薬学部, 准教授 (30305495)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
ADACHI Tetsuo 岐阜薬科大学, 薬学部, 教授 (40137063)
KAMIYA Tetsuro 岐阜薬科大学, 薬学部, 助教 (60453057)
|
|---|
| Project Period (FY) |
2011 – 2013
|
| Project Status |
Completed (Fiscal Year 2013)
|
| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
|
|---|
| Keywords | 亜鉛 / 脳梗塞 / 神経細胞死 / アポトーシス / スプライシング / 脳虚血 |
|---|
| Research Abstract |
There is increasing evidence that excessive zinc release from presynaptic terminals following cerebral ischemia induces neuronal cell death. It was reported that the blockade of free zinc by zinc chelators abolishes the neurodegeneration induced by cerebral ischemia. These findings support the concept that zinc is one of mediators of ischemic neuronal cell death. However, the mechanism is not fully understood. In this study, we addressed molecular mechanisms of zinc-induced neurotoxicity. We demonstrated here that zinc-induced apoptosis might be regulated, at least in part, through alterations in splicing pattern of pro-apoptotic factor Bim. To our knowledge, this is first report showing a novel function of zinc as a splicing regulator. In addition, we provided evidence that apomorphine, a dopamine receptor agonist, protects against zinc-induced neurotoxicity independently of dopamine receptors.
|
Report
(4 results)
Research Products
(32 results)
-
[Journal Article] Newly Synthesized ‘Hidabeni’ Chalcone Derivatives Potently Suppress LPS-Induced NO Production <i>via</i> Inhibition of STAT1, but Not NF-κB, JNK, and p38, Pathways in Microglia2014
Author(s)
Hara H, Ikeda R, Ninomiya M, Kamiya T, Koketsu M, Adachi T
-
Journal Title
Biological and Pharmaceutical Bulletin
Volume: 37
Issue: 6
Pages: 1042-1049
DOI
NAID
ISSN
0918-6158, 1347-5215
Related Report
Peer Reviewed
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
