Treatment with the molecular mechanism analysis of myocardial cell protection in myocardial infarction
| Project/Area Number |
25860628
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Kurume University |
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Principal Investigator |
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| Research Collaborator |
YASUKAWA Hideo
OBA Toyoharu
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | Sprouty4 / 急性心筋梗塞 |
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| Outline of Final Research Achievements |
It has been shown that ERK1/2 signaling pathway has protective role in the development of left ventricular (LV) remodeling after acute myocardial infarction (AMI). However, little is known about the role of negative regulator of ERK1/2 signaling pathway in the process of LV remodeling after AMI. We have shown that Sprouty4 (Spry4) is an intrinsic negative regulator of ERK1/2 signaling pathway in pathophysiology including angiogenesis. In this study, we determined whether ERK1/2 suppressor Spry4 would play a role in the development of LV remodeling after AMI.
The ERK1/2-Spry4 pathway is activated in the development of LV remodeling after AMI. The ERK1/2 phosphorylation and the LV remodeling after AMI are not different between Spry4-KO and WT mice. This study suggests that ERK1/2 suppressor Spry4 does not play an important role in the development of LV remodeling after AMI.
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Report
(3 results)
Research Products
(1 results)
