2009 Fiscal Year Final Research Report
G-protein independent signaling induced by be-ta blocker and the significance of the signaling.
| Project/Area Number |
20790066
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Biological pharmacy
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| Research Institution | Kyushu University |
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Principal Investigator |
NAKAYA Michio Kyushu University, 薬学研究院, 助教 (80464387)
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| Project Period (FY) |
2008 – 2009
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| Keywords | 薬理学 / シグナル伝達 / G蛋白質 |
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| Research Abstract |
Metoprolol is one of antagonists specific for the β1 adrenergic receptor. We accidentally found that long-term administration of metoprolol induced cardiac fibrosis in mice. This fibrosis signal by metoprolol is mediated by β1 adrenergic receptor in a G protein-independent fashion and requires ERK activation. We also demonstrate that the signal pathway depends on β-arrestin2 and GRK5. Indeed, the cardiac fibrosis was not observed when the metoprolol was administered to β-arrestin2 or GRK5 deficient mice.
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[Journal Article] P2Y_6 Receptor-Gα_<12/13> Signaling in Cardiomyocytes Triggers Pressure Overload-induced Cardiac Fibrosis.2008
Author(s)
Nishida M, Sato Y, Uemura A, Narita Y, Tozaki-Saitoh H, Nakaya M, Ide T, Suzuki K, Inoue K, Nagao T, Kurose H
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Journal Title
EMBO J. 27
Pages: 3104-3115
Peer Reviewed
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