| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Outline of Final Research Achievements |
Left ventricular (LV) remodeling following myocardial infarction (MI) has an important role on global cardiac function. Muscle atrophy F-box (MAFbx), an E3 ubiquitin ligase, induces skeletal muscle atrophy and cardiac remodeling under the condition of pressure overload, but the roles of MAFbx in MI is not well understood. Our aim is to determine if MAFbx contribute to cardiac remodeling following MI. MAFbx-knockout (KO) and wild-type (WT) mice were subjected to permanent coronary ligation to create MI. The infarct sizes 3 days after MI were not significantly different in WT and MAFbx KO mice. In comparison with WT mice, MAFbx KO mice were protected against early mortality due to cardiac rupture. MMP9 activity in risk areas 3 days after MI was significantly reduced in KO mice than in WT mice.
MAFbx protein level increase in acute phase after MI. Gene deletion of MAFbx deletion reduces mortality after MI and cardiac rupture, decreasing the activity of MMP9.
|
