Fatty acid incorporation is decreased in astrocytes cultured from alpha-synuclein gene-ablated mice.
J Neurochem
; 94(3): 839-49, 2005 Aug.
Article
in En
| MEDLINE
| ID: mdl-16033426
ABSTRACT
Because alpha-synuclein may function as a fatty acid binding protein, we measured fatty acid incorporation into astrocytes isolated from wild-type and alpha-synuclein gene-ablated mice. alpha-Synuclein deficiency decreased palmitic acid (160) incorporation 31% and arachidonic acid [204 (n-6)] incorporation 39%, whereas 226 (n-3) incorporation was unaffected. In neutral lipids, fatty acid targeting of 204 (n-6) and 226 (n-3) (docosahexaenoic acid) to the neutral lipid fraction was increased 1.7-fold and 1.6-fold, respectively, with an increase in each of the major neutral lipids. This was consistent with a 3.4- to 3.8-fold increase in cholesteryl ester and triacylglycerol mass. In the phospholipid fraction, alpha-synuclein deficiency decreased 160 esterification 39% and 204 (n-6) esterification 43% and decreased the distribution of these fatty acids, including 226 (n-3), into this lipid pool. alpha-Synuclein gene-ablation significantly decreased the trafficking of these fatty acids to phosphatidylinositol. This observation is consistent with changes in phospholipid fatty acid composition in the alpha-synuclein-deficient astrocytes, including decreased 226 (n-3) content in the four major phospholipid classes. In summary, these studies demonstrate that alpha-synuclein deficiency significantly disrupted astrocyte fatty acid uptake and trafficking, with a marked increase in fatty acid trafficking to cholesteryl esters and triacylglycerols and decreased trafficking to phospholipids, including phosphatidylinositol.
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Collection:
01-internacional
Database:
MEDLINE
Main subject:
Astrocytes
/
Fatty Acids
/
Nerve Tissue Proteins
Limits:
Animals
Language:
En
Journal:
J Neurochem
Year:
2005
Document type:
Article
Affiliation country:
United States