| Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Outline of Final Research Achievements |
Suppressor of cytokine signaling-3 (SOCS3) is a cytokine-inducible negative regulator of JAK-STAT signaling pathway. Cardiac-specific SOCS3 deficient mice (SOCS3-CKO) spontaneously develop cardiac dysfunction with advanced age. In this study, we analysed the underlying mechanism of age-related cardiac dysfunction in SOCS3-cKO mice. We found that developed cardiac dysfunction estimated by echocardiogram and increased activation of STAT3 from 25 weeks of age in SOCS3-CKO. In SOCS3-CKO mice hearts from 25 weeks of age, LC3II/LC3I ratio was significantly decreased. Western blot analysis revealed that expression of parkin and PINK1 but not p62 and Bnip3 were decreased in SOCS3-CKO mice compared with control mice from 25 weeks of age. These results suggest that age-related cardiac dysfunction in SOCS3-CKO mice may be due to impaired autophagy through sustained STAT3 activation.
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