The role of beta adrenergic signaling in fibroblasts during cardiac senescence
| Project/Area Number |
17K09576
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cardiovascular medicine
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| Research Institution | Osaka University |
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Principal Investigator |
NAKAYAMA Hiroyuki 大阪大学, キャンパスライフ健康支援センター, 招へい准教授 (40581062)
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| Co-Investigator(Kenkyū-buntansha) |
種池 学 大阪大学, キャンパスライフ健康支援センター, 助教 (30609756)
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| Project Period (FY) |
2017-04-01 – 2020-03-31
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| Project Status |
Completed (Fiscal Year 2019)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 心臓老化 / 線維芽細胞 / アドレナリン受容体 / 老化 / 心肥大 / 循環器・高血圧 |
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| Outline of Final Research Achievements |
This study was designed to verify a hypothesis that aging-related cardiomyopathy (ARC) would be developed due to chronic inflammation based on the relation between sympathetic nerve and inflammation in cardiac fibroblasts. We used beta 2 adrenergic receptor knockout (β2ARKO) mice for this study and observed a shortness of life, a decrease in left ventricular diastolic function and an increase in cardiac fibrosis in accordance with age, compared to control mice. On the other hand, there was no significant difference between aged control and β2ARKO mice in senescence-associated secreted phenotypes. Those results were different from the hypothesis and suggested that β2AR might have a protective role in the development of ARC due to cardiac diastolic dysfunction with fibrosis.
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| Academic Significance and Societal Importance of the Research Achievements |
本研究において、β2アドレナリン受容体欠失に伴い、マウスの寿命が短縮したことから、β2アドレナリン受容体を活性化させることにより、寿命を延長する可能性があることが示唆された。また、β2アドレナリン受容体は、心臓において拡張能の維持を介してaging-related cardiomyopathyを抑制することが明らかとなった。β2アドレナリン受容体アゴニストは気管支喘息に対する治療として貼付剤が一般的に使用されており、この既存の薬剤が健康寿命を延長させる治療へ展開できる可能性を示唆している。
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Report
(4 results)
Research Products
(12 results)
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[Journal Article] Myofibroblast β2 adrenergic signaling amplifies cardiac hypertrophy in mice.2019
Author(s)
1.Imaeda A, Tanaka S, Tonegawa K, Fuchigami S, Obana M, Maeda M, Kihara M, Kiyonari H, Conway SJ, Fujio Y, Nakayama H.
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Journal Title
Biochem Biophys Res Commun.
Volume: 510
Issue: 1
Pages: 149-155
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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[Journal Article] Phospholamban inhibition by a single dose administration of locked nucleic acid antisense oligonucleotide improves cardiac contractility in pressure overload-induced systolic dysfunction in mice.2017
Author(s)
Morihara, H., Yamamoto, T., Oiwa, H., Tonegawa, K., Tsuchiyama, D., Kawakatsu, I., Obana, M., Maeda, M., Mohri, T., Obika, S., Fujio, Y., Nakayama, H.
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Journal Title
J. Cardiovasc. Pharmacol. Ther.
Volume: 印刷中
Issue: 3
Pages: 273-282
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] 2-aminoethoxydiphenyl borate provides an anti-oxidative effect and mediates cardioprotection during ischemia reperfusion in mice.2017
Author(s)
Morihara H, Obana M, Tanaka S, Kawakatsu I, Tsuchiyama D, Mori S, Suizu H, Ishida A, Kimura R, Tsuchimochi I, Maeda M, Yoshimitsu T, Fujio Y, Nakayama H.
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Journal Title
PLoS One.
Volume: 12
Issue: 12
Pages: e0189948-e0189948
DOI
Related Report
Peer Reviewed / Open Access
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