Immunobiological analysis of cardiac muscle type ryanodine receptor genetic mutation mice
| Project/Area Number |
24890282
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Legal medicine
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| Research Institution | Hyogo Medical University |
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Principal Investigator |
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| Project Period (FY) |
2012-08-31 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | RyR2 / 突然死 / 胸腺 / 心電図 / 遺伝子組換えマウス / miRNA / 遺伝子改変マウス |
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| Research Abstract |
In this study, we investigated whether the R420W mutation of RyR2 is associated with the phenotypic characteristics of status thymicolymphaticus by generating a knock-in mouse model carrying the mutation. Homozygous (RyR2R420W/R420W) mice showed significant increases in thymus and spleen weights, when compared with wild-type mice. In addition, various types of arrhythmias were induced in RyR2R420W/R420W mice in response to the administration of caffeine and adrenaline; the same results were not observed in wild-type mice. These findings suggest that RyR2R420W/R420W mice exhibit status thymicolymphaticus-like phenotypes. This mouse model may be useful for studying the pathophysiology of this condition. The amount of mmu-miR-291b-5p from the thymus and spleen decreased in the RyR2R420W/R420W mice. These results suggested that mmu-miR-291b-5p possible may be associated with the pathophysiological process leading to the hypertrophy of lymphoid organs.
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Report
(3 results)
Research Products
(6 results)
