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Int. J. Mol. Sci. 2017, 18(8), 1636; doi:10.3390/ijms18081636

A Novel Perspective on the ApoM-S1P Axis, Highlighting the Metabolism of ApoM and Its Role in Liver Fibrosis and Neuroinflammation

1
Department of Clinical Biochemistry, University Hospital of Copenhagen, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark
2
Department of Biomedical Sciences, Faculty of Health and Science, University of Copenhagen, Blegdamsvej 3, 2200 Copenhagen, Denmark
3
Department of Cardiology, University Hospital of Copenhagen, Rigshospitalet, Blegdamsvej 9, 2100 Copenhagen, Denmark
*
Author to whom correspondence should be addressed.
Received: 29 June 2017 / Revised: 18 July 2017 / Accepted: 25 July 2017 / Published: 27 July 2017
(This article belongs to the Special Issue Sphingolipids: Signals and Disease)
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Abstract

Hepatocytes, renal proximal tubule cells as well as the highly specialized endothelium of the blood brain barrier (BBB) express and secrete apolipoprotein M (apoM). ApoM is a typical lipocalin containing a hydrophobic binding pocket predominantly carrying Sphingosine-1-Phosphate (S1P). The small signaling molecule S1P is associated with several physiological as well as pathological pathways whereas the role of apoM is less explored. Hepatic apoM acts as a chaperone to transport S1P through the circulation and kidney derived apoM seems to play a role in S1P recovery to prevent urinal loss. Finally, polarized endothelial cells constituting the lining of the BBB express apoM and secrete the protein to the brain as well as to the blood compartment. The review will provide novel insights on apoM and S1P, and its role in hepatic fibrosis, neuroinflammation and BBB integrity. View Full-Text
Keywords: apolipoprotein M; Sphingoshine-1-Phosphate; lipid metabolism; liver fibrosis; blood brain barrier apolipoprotein M; Sphingoshine-1-Phosphate; lipid metabolism; liver fibrosis; blood brain barrier
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Hajny, S.; Christoffersen, C. A Novel Perspective on the ApoM-S1P Axis, Highlighting the Metabolism of ApoM and Its Role in Liver Fibrosis and Neuroinflammation. Int. J. Mol. Sci. 2017, 18, 1636.

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