Por favor, use este identificador para citar o enlazar a este item:
http://hdl.handle.net/10261/196850
COMPARTIR / EXPORTAR:
SHARE CORE BASE | |
Visualizar otros formatos: MARC | Dublin Core | RDF | ORE | MODS | METS | DIDL | DATACITE | |
Título: | Myelin extracellular leaflet compaction requires apolipoprotein D membrane management to optimize lysosomal‐dependent recycling and glycocalyx removal |
Autor: | García-Mateo, Nadia CSIC; Pascua-Maestro, Raquel CSIC ORCID; Pérez-Castellanos, Alberto CSIC ORCID; Lillo, Concepción; Sánchez, Diego CSIC ORCID CVN; Ganfornina, M. D. CSIC ORCID CVN | Fecha de publicación: | 2018 | Editor: | Wiley-VCH | Citación: | Glia 66(3): 670-687 (2018) | Resumen: | To compact the extracellular sides of myelin, an important transition must take place: from membrane sliding, while building the wraps, to membrane adhesion and water exclusion. Removal of the negatively charged glycocalyx becomes the limiting factor in such transition. What is required to initiate this membrane‐zipping process? Knocking‐out the Lipocalin Apolipoprotein D (ApoD), essential for lysosomal functional integrity in glial cells, results in a specific defect in myelin extracellular leaflet compaction in peripheral and central nervous system, which results in reduced conduction velocity and suboptimal behavioral outputs: motor learning is compromised. Myelination initiation, growth, intracellular leaflet compaction, myelin thickness or internodal length remain unaltered. Lack of ApoD specifically modifies Plp and P0 protein expression, but not Mbp or Mag. Late in myelin maturation period, ApoD affects lipogenic and growth‐related, but not stress‐responsive, signaling pathways. Without ApoD, the sialylated glycocalyx is maintained and ganglioside content remains high. In peripheral nervous system, Neu3 membrane sialidase and lysosomal Neu1 are coordinately expressed with ApoD in subsets of Schwann cells. ApoD‐KO myelin becomes depleted of Neu3 and enriched in Fyn, a kinase with pivotal roles in transducing axon‐derived signals into myelin properties. In the absence of ApoD, partial permeabilization of lysosomes alters Neu1 location as well. Exogenous ApoD rescues ApoD‐KO hypersialylated glycocalyx in astrocytes, demonstrating that ApoD is necessary and sufficient to control glycocalyx composition in glial cells. By ensuring lysosomal functional integrity and adequate subcellular location of effector and regulatory proteins, ApoD guarantees the glycolipid recycling and glycocalyx removal required to complete myelin compaction. | Versión del editor: | https://doi.org/10.1002/glia.23274 | URI: | http://hdl.handle.net/10261/196850 | DOI: | 10.1002/glia.23274 | ISSN: | 0894-1491 | E-ISSN: | 1098-1136 |
Aparece en las colecciones: | (IBGM) Artículos |
Ficheros en este ítem:
Fichero | Descripción | Tamaño | Formato | |
---|---|---|---|---|
myelinremoval.pdf | 2,34 MB | Adobe PDF | Visualizar/Abrir |
CORE Recommender
PubMed Central
Citations
19
checked on 17-abr-2024
SCOPUSTM
Citations
24
checked on 15-abr-2024
WEB OF SCIENCETM
Citations
23
checked on 27-feb-2024
Page view(s)
187
checked on 23-abr-2024
Download(s)
180
checked on 23-abr-2024