2013 Fiscal Year Final Research Report
Clarification of mechanisms underlying the enlargement of intracranial aneurysms focused on drop-out of medial smooth muscle cells.
Project/Area Number |
24890097
|
Research Category |
Grant-in-Aid for Research Activity Start-up
|
Allocation Type | Single-year Grants |
Research Field |
Cerebral neurosurgery
|
Research Institution | Kyoto University |
Principal Investigator |
AOKI TOMOHIRO 京都大学, 医学(系)研究科(研究院), 准教授 (40633144)
|
Project Period (FY) |
2012-08-31 – 2014-03-31
|
Keywords | 脳動脈瘤 / 細胞外基質 / 炎症反応 / マクロファージ / 脂質 / TNF-alpha |
Research Abstract |
Intracranial aneurysm (IA) is a major cause of subarachnoid hemorrhage (SAH), the most severe form of stroke.Histologically, IA is characterized as a lesion with excessive degenerative changes of arterial walls. However, the mechanisms regulating such degenerative changes of the media remains to be elucidated. In the present study, we have revealed the crucial role of inflammatory responses in IA formation, especially the degenerative changes of the media, mainly using rodent models of IAs. Further, in series of studies, we have clarified some potential mediators regulating or positively correlated with degeneration, such as lipid accumulation in adventitia of IA walls, prostaglandin F2a-FP signaling cascade and TNF-alpha signaling. In conclusion, the findings from the present study have suggested the role of inflammatory responses in degenerative changes in IA lesions.
|