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

  • Wang, MinThird Affiliated Hospital of Soochow University (författare)

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

  • Artikel/kapitelEngelska2019

Förlag, utgivningsår, omfång ...

  • Spandidos Publications Ltd,2019
  • 12 s.

Nummerbeteckningar

  • LIBRIS-ID:oai:lup.lub.lu.se:1b8e7c7b-a775-4099-bac1-db443a0d3e3d
  • https://lup.lub.lu.se/record/1b8e7c7b-a775-4099-bac1-db443a0d3e3dURI
  • 10.3892/mmr.2018.9747DOI

Kompletterande språkuppgifter

  • Språk:engelska
  • Sammanfattning på:engelska

Ingår i deldatabas

Klassifikation

  • Ämneskategori:ref swepub-contenttype
  • Ämneskategori:art swepub-publicationtype

Anmärkningar

  • © 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 och genrebeteckningar

Biuppslag (personer, institutioner, konferenser, titlar ...)

  • Luo, Guang HuaThird Affiliated Hospital of Soochow University (författare)
  • Liu, HongThird Affiliated Hospital of Soochow University (författare)
  • Zhang, You PuThird Affiliated Hospital of Soochow University (författare)
  • Wang, BinThird Affiliated Hospital of Soochow University (författare)
  • Di, Dong MeiThird Affiliated Hospital of Soochow University (författare)
  • Zhan, Xiang HongThird Affiliated Hospital of Soochow University (författare)
  • Yu, YangThird Affiliated Hospital of Soochow University (författare)
  • Yao, ShuangThird Affiliated Hospital of Soochow University (författare)
  • Zhang, Xiao YingThird Affiliated Hospital of Soochow University (författare)
  • Xu, NingLund 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(Swepub:lu)kkem-nxu (författare)
  • Third Affiliated Hospital of Soochow UniversityAvdelningen för klinisk kemi och farmakologi (creator_code:org_t)

Sammanhörande titlar

  • Ingår i:Molecular Medicine Reports: Spandidos Publications Ltd19:2, s. 1272-12831791-2997

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