Exploration for the detailed mechanism of subarachnoid hemorrhage-induced white matter injury.
| Project/Area Number |
15H06248
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Neurosurgery
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| Research Institution | Gifu University |
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Principal Investigator |
EGASHIRA Yusuke 岐阜大学, 大学院医学系研究科, 助教 (50547677)
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 白質傷害 / クモ膜下出血 / 血液脳関門 / SAH |
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| Outline of Final Research Achievements |
The detailed mechanism of white matter (WM) injury after subarachnoid hemorrhage (SAH) remains unclear. We hypothesized that blood-brain barrier (BBB) disruption occurs in WM after SAH and it leads to consequent injury. SAH was induced by endovascular perforation in male mice. In SAH mice, BBB leakage along the WM was observed at 24 h after SAH. In microvessels, tight junction detachment and swollen asrtocyte endfeet were demonstrated by electron microscopy. Matirx metalloproteinase (MMP)-9 activity and lipocalin (LCN)-2 expression were increased in the WM at the acute stage of SAH. At 8 days after SAH, decreased myelin integrity and an increased density of damaged axon were observed in SAH mice. MMP-9 or LCN-2 deletion effectively suppressed this SAH-induced WM injury. In conclusion, SAH causes BBB disruption and consequent injury in the WM, and MMP-9 and LCN-2 play an important role for those pathologies. These factors could be a novel therapeutic target for SAH-induced WM injury.
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Report
(3 results)
Research Products
(8 results)
