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Sökning: onr:"swepub:oai:lup.lub.lu.se:1b8e7c7b-a775-4099-bac1-db443a0d3e3d" > Apolipoprotein M in...

Apolipoprotein M induces inhibition of inflammatory responses via the S1PR1 and DHCR24 pathways

Wang, Min (författare)
Third Affiliated Hospital of Soochow University
Luo, Guang Hua (författare)
Third Affiliated Hospital of Soochow University
Liu, Hong (författare)
Third Affiliated Hospital of Soochow University
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Zhang, You Pu (författare)
Third Affiliated Hospital of Soochow University
Wang, Bin (författare)
Third Affiliated Hospital of Soochow University
Di, Dong Mei (författare)
Third Affiliated Hospital of Soochow University
Zhan, Xiang Hong (författare)
Third Affiliated Hospital of Soochow University
Yu, Yang (författare)
Third Affiliated Hospital of Soochow University
Yao, Shuang (författare)
Third Affiliated Hospital of Soochow University
Zhang, Xiao Ying (författare)
Third Affiliated Hospital of Soochow University
Xu, Ning (författare)
Lund University,Lunds universitet,Avdelningen för klinisk kemi och farmakologi,Institutionen för laboratoriemedicin,Medicinska fakulteten,Division of Clinical Chemistry and Pharmacology,Department of Laboratory Medicine,Faculty of Medicine
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 (creator_code:org_t)
Spandidos Publications Ltd, 2019
2019
Engelska 12 s.
Ingår i: Molecular Medicine Reports. - : Spandidos Publications Ltd. - 1791-2997. ; 19:2, s. 1272-1283
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • © 2019 Spandidos Publications. All rights reserved. Apolipoprotein M (ApoM) is a type of apolipoprotein. It is well known that high-density lipoprotein (HDL) decreases inflammatory responses via the apoM-sphingosine-1-phosphate (S1P) pathway. The present study further investigated the importance of ApoM in the inhibitory effects of HDL on inflammation. Mice with an apoM gene deficiency (apoM-/-) were employed to investigate the effects of ApoM on the expression of interleukin-1β (IL-1β), monocyte chemotactic protein-1 (MCP-1), S1P receptor-1 (S1PR1) and 3β-hydroxysterol Δ-24-reductase (DHCR24), as compared with in wild-type mice (apoM+/+). Furthermore, cell culture experiments were performed using a permanent human hybrid endothelial cell line (EA.hy926). Cells were cultured in the presence of recombinant human apoM (rec-apoM) or were induced to overexpress apoM (apoMTg); subsequently, cells were treated with tumor necrosis factor-α (TNF-α), in order to investigate the effects of ApoM on IL-1β and MCP-1. The results demonstrated that the mRNA expression levels of IL-1β and MCP-1 were significantly higher in the liver following administration of lipopolysaccharide in apoM-/- mice compared with in apoM+/+ mice. In cell culture experiments, when cells were pre-cultured with rec-apoM or were engineered to overexpress apoM (apoMTg), they exhibited decreased expression levels of IL-1β and MCP-1 following TNF-α treatment compared with in normal apoM-expressing cells (apoMTgN). Furthermore, the mRNA expression levels of IL-1β and MCP-1 were significantly elevated following addition of the S1PR1 inhibitor W146, but not by the scavenger receptor class B type I inhibitor, block lipid transport-1 (BLT-1), in apoMTg cells prior to TNF-α treatment. Conversely, there were no differences in these inflammatory biomarkers under the same conditions in apoMTgN cells. The mRNA expression levels of DHCR24 were significantly reduced by the addition of BLT-1 prior to TNF-α treatment in apoMTg cells; however, there was no difference in the expression of this inflammatory biomarker in apoMTgN cells. In conclusion, ApoM displayed inhibitory effects against the inflammatory response in vivo and in vitro; these effects may be induced via the S1PR1 and DHCR24 pathways.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Cell- och molekylärbiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Cell and Molecular Biology (hsv//eng)
MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine (hsv//eng)

Nyckelord

3β-hydroxysterol Δ-24-reductase
Apolipoprotein M
High-density lipoprotein
Interleukin-1β
Monocyte chemotactic protein-1
Sphingosine-1-phosphate
Vascular inflammation

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