| Project/Area Number |
12671363
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Cerebral neurosurgery
|
|---|
| Research Institution | The University of Tokushima |
|---|
Principal Investigator |
NAGAHIRO Shinji The University of Tokushima, School of Medicine, Professor, 医学部, 教授 (60145315)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
MATSUBARA Shunji The University of Tokushima, School of Medicine, Research Associate, 医学部, 助手 (60294675)
SATOH Koichi The University of Tokushima, University Hospital, 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)
|
|---|
| Project Period (FY) |
2000 – 2001
|
| Project Status |
Completed (Fiscal Year 2001)
|
| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2000: ¥1,600,000 (Direct Cost: ¥1,600,000)
|
|---|
| Keywords | cerebral aneurvsm / smooth muscle cell / phenotypic modulation / myosin heavy chain isoforms / BTEB2 / macrophage |
|---|
| Research Abstract |
The growth and rupture mechanisms of cerebral aneurysms are still unknown. We used immunohistochemical methods to determine the role of phenotypically modulated smooth muscle cells (SMCs) in the growth and rupture of cerebral aneurysms. Materials and Methods : Aneurysmal wall specimens (N=58) were obtained at operation or autopsy, and 12 control cerebral arteries were obtained at autopsy. Semiserial sections were subjected to immunohistochemical staining with antibodies to α -smooth muscle actin (α -SMA), desmin, smooth muscle myosin heavy chain isoforms (SM1 , SM2 and SMemb), macrophages and basic transcription regulatory binding protein 2 (BTEB2) which regulates the induction of the gene for SMemb. In control cerebral arteries, SMCs in the media was strongly immunostained for α -SMA, desmin, SM1 and SM2 ; immunoreactivity for SMemb was faint. SMCs in both unruptured and ruptured aneurysmal walls showed no staining of desmin; the expression of α -SMA was well preserved, the expression of SMemb was increased in 30 % of unruptured aneurysms, although the expression of SM2 and SMemb was decreased in all ruptured aneurysms. The expression of BTEB2 was increased in macrophages and SMCs in the large to grant unruptured aneurysms: it was not seen in ruptured aneurysms exhibiting macrophage infiltration. Our study suggests that SMCs in aneurysmal walls are phenotypically different from the contractile type in the media of normal cerebral arteries. In some unruptured aneurysms, at least some SMCs are of the synthetic type. The up-regulation of BTEB2 in macrophages and SMCs appears to the related to aneurysmal growth. SMCs in ruptured aneurysms may have lost both phenotypes (contractyle and synthetic) before rupture.
|
