Journal
GLIA
Volume 66, Issue 2, Pages 327-347Publisher
WILEY
DOI: 10.1002/glia.23245
Keywords
demyelination; lysolecithin; multiple sclerosis; myelin; oligodendrocyte
Categories
Funding
- Canadian Institutes for Health Research (CIHR)
- MS Society of Canada
- Alberta Heritage Foundation For Medical Research
- CRIO Team grant from Alberta Innovates Health Solutions (AIHS)
- CIHR
- University of Calgary
- AIHS
- Vanier Canada Graduate Scholarship
- University of Calgary, Faculty of Medicine
- Canada Research Chair awards
- Alberta Innovates [201300669, 201400502, 201500411, 201500417] Funding Source: researchfish
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For decades lysophosphatidylcholine (LPC, lysolecithin) has been used to induce demyelination, without a clear understanding of its mechanisms. LPC is an endogenous lysophospholipid so it may cause demyelination in certain diseases. We investigated whether known receptor systems, inflammation or nonspecific lipid disruption mediates LPC-demyelination in mice. We found that LPC nonspecifically disrupted myelin lipids. LPC integrated into cellular membranes and rapidly induced cell membrane permeability; in mice, LPC injury was phenocopied by other lipid disrupting agents. Interestingly, following its injection into white matter, LPC was cleared within 24 hr but by five days there was an elevation of endogenous LPC that was not associated with damage. This elevation of LPC in the absence of injury raises the possibility that the brain has mechanisms to buffer LPC. In support, LPC injury in culture was significantly ameliorated by albumin buffering. These results shed light on the mechanisms of LPC injury and homeostasis.
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