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First published online April 1, 2009

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LRP1 – quick on the (myelin) uptake

The degradation of the myelin sheath that surrounds neurons is a key feature of multiple sclerosis (MS), and the presence of degraded myelin in the extracellular space is thought to be pathogenic; thus, its internalisation by CNS cells might modify disease progression. Now, Steven Gonias and colleagues (p. 1155) identify low-density liporotein receptor-related protein 1 (LRP1) as an important receptor for the phagocytosis of degraded myelin. Using myelin vesicles (MVs) as a model of degraded myelin, the authors first show that these are internalised by mouse embryonic fibroblasts only when the cells express LRP1; moreover, uptake is blocked by receptor-associated protein (RAP), which prevents the interaction of LRP1 with other ligands. The authors next prepare primary cultures of oligodendrocytes, astrocytes and microglia, and show that all three cell types express LRP1, and internalise MVs when RAP is absent. In vitro, myelin basic protein (MBP; a major myelin component) binds to LRP1, and a MBP-specific antibody inhibits MV internalisation by oligodendrocytes. Finally, the authors report that LRP1 expression is increased in the CNS of mice with experimental autoimmune encephalomyelitis (an established model of MS). On the basis of their results, the authors propose that LRP1 might function as an important regulator of MS progression.

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Low-density lipoprotein receptor-related protein 1 is an essential receptor for myelin phagocytosis

Alban Gaultier, Xiaohua Wu, Natacha Le Moan, Shinako Takimoto, Gatambwa Mukandala, Katerina Akassoglou, W. Marie Campana, and Steven L. Gonias
JCS 2009 122: 1155-1162. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?