Search for novel therapeutic methods for anti-MAG antibody related neuropathy based on microvascular pathology
Project/Area Number |
15K15340
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Research Category |
Grant-in-Aid for Challenging Exploratory Research
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Allocation Type | Multi-year Fund |
Research Field |
Neurology
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Research Institution | Yamaguchi University |
Principal Investigator |
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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Keywords | 抗MAG抗体関連ニューロパチー / 血液神経関門 / IgM型抗MAG抗体関連ニューロパチー / インヴィトロモデル / ニューロパチー |
Outline of Final Research Achievements |
To reveal the pathology of blood-nerve barrier (BNB) disruption in anti-myelin associated glycoprotein (MAG) antibody related neuropathy, we performed in vitro study using human BNB model. IgM antibody derived from anti-MAG antibody-related neuropathy decreased the barrier function of monolayer-cultured endothelial cells. Myelin protein zero (MPZ) and peripheral myelin protein 22 (PMP 22) are present in cell lines of endothelial cells and pericytes established from human peripheral nerve microvasculature. The anti-MAG antibody may be involved in BNB dysfunction by targeting the molecules which carrier carbohydrate HNK-1 epitope existing on endothelial cells and pericytes constituting BNB.
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Report
(4 results)
Research Products
(7 results)