| Project/Area Number |
13671439
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | The University of Tokushima |
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Principal Investigator |
NAKAJIMA Norito The University of Tokushima, School of Medicine, Assistant, 医学部附属病院, 助手 (00332817)
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| Co-Investigator(Kenkyū-buntansha) |
ISATOH Koichi The University of Tokushima, School of Medicine, Assistant Professor, 医学部附属病院, 講師 (90225938)
SANO Toshiaki The University of Tokushima, School of Medicine, Professor, 医学部, 教授 (80154128)
NAGAHIRO Shinji The University of Tokushima, School of Medicine, Professor, 医学部, 教授 (60145315)
松原 俊二 徳島大学, 医学部, 助手 (60294675)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2001: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | cerebral aneurysm / smooth muscle cell / macrophage / BTEB2 / 脳動脈癌 |
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| Research Abstract |
Introduction: Smemb, which is known increase in synthetic smooth muscle cells (SMCs). The induction of the gene for Smemb is regulated by basic transcription regulatory element binding protein 2 (BTEB2). In the current study we investigated the expression of BTEB2 in the aneurysm to determine its role in aneurysmail development and in protection against wall rupture.
Methods: Non-ruptured aneurysms (n=15) and ruptured aneurysms (n=12) were obtained at surgery or autopsy. Five control arteries were obtained at autopsy. The spesimens were stained immunohistochemically with antibodies to a-smooth muscle actin, macrophages and BTEB2.
Results: In control cerebral arteries, SMCs in the media and macrophages in the adventitia were negative for BTEB2. In 7 of 9 non-ruptured aneurysms larger than 10 mm, but not in any of the small non-ruptured aneurysms, macrophages and SMCs in the luminal layer were positive for BTEB2. And in thrombus of non-ruptured giant aneurysms, SMCs migrated and macrophages were strongly positive for BTEB2. With the exception of a few large or giant aneurysms, in ruptured aneurysms, macrophages and SMCs in the luminal layer were negative for BTEB2.
Conclusion: In our study, BTEB2-positive macrophages and SMCs were present in the luminal layer of larger and giant non-ruptured aneurysms. This suggests that BTEB2 expression in the aneurysmal wall is related to aneurismal growth and may against rupture.
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