2017 Fiscal Year Final Research Report
Pathogenic mechanism of spontaneous hypertensive intracerebral hemorrhage focused on ROS-producing enzyme Nox4 expressed in brain microvascular pericytes
| Project/Area Number |
26462163
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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 |
Neurosurgery
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Research Collaborator |
AGO Tetsuro 九州大学, 大学病院, 講師 (30514202)
KURODA Junya 九州大学, 大学病院, 助教 (70614858)
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| Project Period (FY) |
2014-04-01 – 2018-03-31
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| Keywords | 脳出血 / 脳卒中 / 高血圧 / 酸化ストレス |
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| Outline of Final Research Achievements |
Brain microvasular pericytes plays a pivotal role in blood-brain barrier (BBB) maintenance. We did not succeed in developing spontaneous intracerebral hemorrhage model through angiotensin II-mediated hypertension in aged mice with overexpression of Nox4, an enzyme producing reactive oxygen species, in pericytes. However, we found that 1) Nox4 expression was upregulted through angiotensin II stimulus in cultured brain pericytes, and that 2) Nox4 overexpression in cultured brain pericytes upregulated expression and activity of NFkB and MMP-9, both of which are highly associated with BBB breakdown. Our results may indicate that Nox4 upregulation in brain pericytes could be one of possible mechanism for hypertensive ntracerebral hemorrhage.
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| Free Research Field |
脳血管障害
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