Ninjurin1 is expressed in myeloid cells and mediates endothelium adhesion in the brains of EAE rats

被引:58
作者
Ahn, Bum Ju [1 ,3 ]
Lee, Hyo-Jong [1 ,3 ]
Shin, Min Wook [1 ,3 ]
Choi, Jeong-Hyun [1 ,3 ]
Jeong, Joo-Won [4 ]
Kim, Kyu-Won [1 ,2 ]
机构
[1] Seoul Natl Univ, Coll Pharm, NeuroVasc Coordinat Res Ctr, Seoul 151742, South Korea
[2] Seoul Natl Univ, Grad Sch Convergence Sci & Technol, Dept Mol Med & Biopharmaceut Sci, Seoul 151742, South Korea
[3] Seoul Natl Univ, Pharmaceut Sci Res Inst, Seoul 151742, South Korea
[4] Kyung Hee Univ, Sch Med, Inst Biomed Sci, Dept Anat & Neurobiol, Seoul 130701, South Korea
关键词
Ninjurin1; Blood-brain barrier; EAE; Multiple sclerosis; Myeloid cell trafficking; MOLECULE; MIGRATION; INJURY;
D O I
10.1016/j.bbrc.2009.07.019
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Ninjurin1 (nerve injury-induced protein, Ninj1) is an adhesion molecule that is essential for cell-to-cell interactions. However. little is known about the function of Ninj1 in the central nervous system (CNS). To address its role in the CNS, we analyzed the expression pattern of Ninj1 in normal rats and in an experimental autoimmune encephalomyelitis (EAE) model. Ninj1 was expressed in three major compartments of brains, meninges, the choroid plexus, and parenchymal perivascular spaces. In the EAE brains, Ninj1 was strongly expressed in myeloid cells (macrophages/monocytes and neutrophils) and partially expressed in endothelial cells (ECs). Furthermore, Ninj1 enhanced adhesion between BV2 cells (murine monocyte lineage microglia) and HBMECs (human brain microvascular endothelial cells). Collectively, our findings suggest that Ninj1 may mediate the entry of myeloid cells into the CNS in normal and EAE brains, and it is a potential therapeutic target for regulating myeloid cell trafficking across the blood-brain barrier (BBB) in CNS immune processes. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:321 / 325
页数:5
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