| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
|---|
| Outline of Final Research Achievements |
In this study, we created smooth-muscle specific SOCS3 (suppressor of cytokine signaling-3) deficient mice (SOCS3-smKO), which is negative feedback regulator of JAK-STAT3 signaling pathway, and investigated the role of SOCS3 in non-cardiomyocyte in diastolic function, cardiac fibrosis, pericardial fibrosis, and post myocardial infarction heart failure. We found that SOCS3-smKO mouse exhibited a variety of phenotypes including diastolic function, pericardial fibrosis, cachexia, and hypotension. The expression of pro-fibrotic CTGF (connective tissue growth factor), PDGFb (platelet growth factor-b), and TGF (transforming growth factor) family genes including TGFb1, TGFb2, and TGFb3, were significantly increased in sm-SOCS3-KO mice hearts. Thus, smooth muscle cell-specific SOCS3 deletion induces increased pericardial fibrosis, cardiac interstitial fibrosis, and increased diastolic dysfunction in aging mice, possibly through the augmentation of pro-fibrotic growth factors.
|
