Insulin-like growth factor binding protein-1 activates integrin-mediated intracellular signaling and migration in oligodendrocytes

被引:26
|
作者
Chesik, Daniel [1 ]
De Keyser, Jacques [1 ,2 ]
Bron, Reinier [1 ]
Fuhler, Gwenny M. [3 ]
机构
[1] Univ Groningen, Univ Med Ctr Groningen, Dept Neurol, NL-9713 GZ Groningen, Netherlands
[2] Univ Hosp Brussels, Dept Neurol, Brussels, Belgium
[3] Univ Groningen, Univ Med Ctr Groningen, Dept Cell Biol, Immunol Sect, NL-9713 GZ Groningen, Netherlands
关键词
insulin-like growth factor; multiple sclerosis; remyelination; CENTRAL-NERVOUS-SYSTEM; HUMAN TROPHOBLAST MIGRATION; IN-VIVO ACTIONS; MULTIPLE-SCLEROSIS; CELL-MIGRATION; IGF-I; ALPHA-5-BETA-1; INTEGRIN; TRANSGENIC MICE; MYELINATION; MYELODYSPLASIA;
D O I
10.1111/j.1471-4159.2010.06703.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
P>In multiple sclerosis (MS), oligodendrocytes in lesions are lost, leaving damaged tissue virtually devoid of these myelin-producing cells. Our group has recently demonstrated enhanced expression of insulin-like growth factor (IGF) binding protein-1 (IGFBP-1) in oligodendrocytes (CNPase+) localized adjacent to MS lesions. In the present study, we demonstrate IGF-1-independent actions of IGFBP-1 on OLN-93 oligodendroglial cells, including activation of kinases ERK1/2, focal adhesion kinase and p21-activated kinase as well as small monomeric GTPases Rac and Ral. Activation of these intracellular signaling components was inhibited by GRGDS peptide, indicating signaling through integrin receptors. While both IGF-1 and IGFBP-1 demonstrated rapid induction of actin polymerization, IGFBP-1 proved to be a more potent inducer of migration than IGF-1, inducing a threefold increased migration rate. Furthermore, through integrin receptor signaling IGFBP-1 induced rapid transient translocalization of intracellular Rac toward punctuated structures followed by translocation of Rac to the plasma membrane. Our results suggest that up-regulation of IGFBP-1 in oligodendrocytes in MS may serve two functions: (i) regulate IGF-1 actions, (ii) exert IGF-independent effects through its RGD sequence.
引用
收藏
页码:1319 / 1330
页数:12
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