| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
Sympathetic hyperactivities have been thought to be a plausible genetic factor responsible for hereditary severe hypertension in stroke-prone spontaneously hypertensive rats (SHRSP). We previously identified stromal interaction molecule 1 (Stim1), in which SHRSP had a nonsense mutation, as a possible candidate gene causally related to exaggerated sympathetic response to stress in SHRSP. In the current study, we created a genome-edited SHRSP which was knocked-in with the wild-type Stim1 by the CRISPR/Cas9 method to investigate whether the functional recovery of STIM1 would mitigate sympatho-excitation to stress in vivo in SHRSP. Unexpectedly, the Stim1 knock-in SHRSP did not show any significant reduction in stress responsiveness (urinary norepinephrine and blood pressure elevation under stress) except for HR under restraint stress condition. In conclusion, the results indicated that Stim1 is not major genetic determinant related to sympathetic hyperresponse to stress in SHRSP.
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