Ninjurin2, a novel homophilic adhesion molecule, is expressed in mature sensory and enteric neurons and promotes neurite outgrowth

被引:117
作者
Araki, T [1 ]
Milbrandt, J [1 ]
机构
[1] Washington Univ, Sch Med, Dept Pathol & Med, Div Lab Med, St Louis, MO 63110 USA
关键词
cell adhesion; postmitotic; peripheral nervous system; hematopoietic and lymphatic organs; chromosome; 12p13; inflammatory bowel disease; acrocallosal syndrome;
D O I
10.1523/JNEUROSCI.20-01-00187.2000
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
A large number of cell adhesion molecules mediate cell-to-cell and cell-to-extracellular matrix interaction during development, differentiation and regeneration of the peripheral nervous system. Here, we report the identification of a novel cell surface adhesion molecule, ninjurin2 (for nerve injury induced protein 2). Ninjurin2 is a homolog of a homophilic cellular adhesion molecule, ninjurin1, that was previously isolated as a gene induced in Schwann cells after nerve injury. Ninjurin1 and 2 share conserved hydrophobic regions for their transmembrane domains; however, they do not contain comparable adhesion motifs nor do they interact with each other. In the peripheral nervous system, ninjurin2 is expressed constitutively in mature sensory and enteric neurons but not in glial cells or in auto-nomic ganglia. Ninjurin2 is upregulated in Schwann cells surrounding the distal segment of injured nerve with a time course similar to that of ninjurin1, neural CAM, and L1. Ninjurin2 promotes neurite outgrowth from primary cultured dorsal root ganglion neurons, presumably via homophilic cellular interactions. Ninjurin2 is also highly expressed in hematopoietic and lymphatic tissues. Finally, the ninjurin2 gene is located on human chromosome 12p13 in which several disorders of unknown etiology have been mapped, including inflammatory bowel disease and acrocallosal syndrome.
引用
收藏
页码:187 / 195
页数:9
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