2002 Fiscal Year Final Research Report Summary
Cerebral endothelial cell and Neurotrophins
| Project/Area Number |
13671177
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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 |
Metabolomics
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| Research Institution | CHIBA UNIVERSITY |
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Principal Investigator |
TATSUNO Ichiro Chiba University, Graduate School of Medicine, Lecturer, 大学院・医学研究院, 講師 (80282490)
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| Co-Investigator(Kenkyū-buntansha) |
SAEKI Naokatsu Chiba University, Graduate School of Medicine, Associate Professor, 大学院・医学研究院, 助教授 (30143275)
UCHIDA Daigaku Chiba University, University Hospital, Assistant, 医学部附属病院, 助手 (80323426)
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| Project Period (FY) |
2001 – 2002
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| Keywords | Cerebral Endothelial cell / Oxidozed LDL / Neurotrophin / Neurotrophin Receptor / Proliferation / NO / PACAP / Cross-talk |
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| Research Abstract |
Cerebral endothelial cells (CEC) are one of the major and key components for formation of the vascular system in the mammalian central nervous system (CNS), which is characteristic and different from that in other organs in terms of the formation of the blood-brain barrier (BBB). Although it has been clarified that both formation and maintenance of the vascular system in CNS are dependent on the cross-talk between neuronal cells and vascular endothelial cells, the precise mechanism is still being investigated. In this regard, we focused on the neurotrophin (NT) produced by neuronal cells for its possible involvement in signaling for the regulation of CEC in comparison of rat cerebral endothelial cells (RCEC) with rat aortic endothelial cells (RAEC). We found that 1) trk C, a receptor for neurotrophin-3 (NT-3), is dominantly expressed in RCEC, but trk B, a receptor for brain-derived neurotrophic factor (BDNF), is dominantly expressed in RAEC ; 2) NT-3 inhibited the proliferation of RCEC ; and 3) NT-3 stimulated the production of nitric oxide (NO) with increases in protein expression of endothelial NO synthase (eNOS). These data indicated that NT may regulate and/or maintain the functions of the brain microvasculature through the regulation of CEC.
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