Cell biology of blood-nerve barrier, using cultured endothelial cell of endoneurial microvessel origin
| Project/Area Number |
10670578
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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 |
Neurology
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| Research Institution | Tokyo Medical and Dental University, Graduate School of Medicine |
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Principal Investigator |
KANDA Takashi Tokyo Medical and Dental University Graduate School, Associate Professor, 医学部, 助教授 (40204797)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1999: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1998: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | blood-nerve barrier (BNB) / blood-brain barrier (BBB) / cytokine / endothelial cell / anti-glycolipid antibody / inflammatory neuropathy / 血管内皮細胞 |
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| Research Abstract |
Penetration of immunoglobulins and/or migration of activated lymphocytes into peripheral nervous system (PNS) parenchyma are the initial key steps to develop immunological disorders of PNS including Guillain-Barre syndrome, IgM neuropathy and chronic inflammatory demyelinating polyradiculoneuropathy. Hence, it is important to know the cellular property of endothelial cells of endoneurial tissue origin (PnMEC) because these cells constitute the bulk of the blood-nerve barrier (BNB). For this purpose we developed a method to isolate and culture pure populations of PnMECs from bovine cauda equina (Kanda T et al., J Neurosci Res 1997) and then established the technique to form in vitro BNB model. Using the BNB in vitro model, we found : (1) endoneurial pericytes enhance the barrier function of this model and may be essential for the BNB integrity (Iwasaki T et al., J Med Dent Sci 1999) ; (2) Various cytokines including VEGF, IL-1 beta, TNF alpha, and TGF beta, which are supposed to play key role in the development of inflammatory neuropathies, are found to decrease the membrane resistance and increase the radioactive tracer (inulin) through this model ; (3) Anti-GM1 monoclonal antibody also weaken the BNB function (Kanda T et al., submitted). Further experiments using sera of neuropathy patients and those to clarify signaling pathways underlying loosening of the BNB following exposure to anti-GM1 antibody are underway.
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Report
(3 results)
Research Products
(17 results)
