Forskning
Udskriv Udskriv
Switch language
Region Hovedstaden - en del af Københavns Universitetshospital
Udgivet

Impaired endothelial barrier function in apolipoprotein M-deficient mice is dependent on sphingosine-1-phosphate receptor 1

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

DOI

  1. Thyroid hormone receptor α in skeletal muscle is essential for T3-mediated increase in energy expenditure

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  2. Influence of FGF23 and Klotho on male reproduction: Systemic vs direct effects

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Preserved capacity for satellite cell proliferation, regeneration, and hypertrophy in the skeletal muscle of healthy elderly men

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  1. Apolipoprotein M and its impact on endothelial dysfunction and inflammation in the cardiovascular system

    Publikation: Bidrag til tidsskriftReviewForskningpeer review

  2. Apolipoprotein M and Sphingosine-1-Phosphate Receptor 1 promote the transendothelial transport of High-Density Lipoprotein

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  3. Increased plasma apoM levels impair triglyceride turnover in mice

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

  4. Oral pre‑treatment with thiocyanate (SCN−) protects against myocardial ischaemia–reperfusion injury in rats

    Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Vis graf over relationer

Apolipoprotein M (ApoM) transports sphingosine-1-phosphate (S1P) in plasma, and ApoM-deficient mice (Apom(-/-)) have ∼50% reduced plasma S1P levels. There are 5 known S1P receptors, and S1P induces adherens junction formation between endothelial cells through the S1P1 receptor, which in turn suppresses vascular leak. Increased vascular permeability is a hallmark of inflammation. The purpose of this study was to explore the relationships between vascular leakage in ApoM deficiency and S1P1 function in normal physiology and in inflammation. Vascular permeability in the lungs was assessed by accumulation of dextran molecules (70 kDa) and was increased ∼40% in Apom(-/-) mice compared to WT (C57Bl6/j) mice. Reconstitution of plasma ApoM/S1P or treatment with an S1P1 receptor agonist (SEW2871) rapidly reversed the vascular leakage to a level similar to that in WT mice, suggesting that it is caused by decreased plasma levels of S1P and reduced S1P1 stimulation. In a carrageenan-induced model of inflammation, Apom(-/-) mice had increased vascular leakage compared with that in WT mice. Adenoviral overexpression of ApoM in Apom(-/-) mice decreased the vascular leakage compared to adenoviral overexpression of green fluorescent protein. The study suggests that vascular leakage of albumin-sized particles in ApoM deficiency is S1P- and S1P1-dependent and this dependency exacerbates the response to inflammatory stimuli.-Christensen, P. M., Liu, C. H., Swendeman, S. L., Obinata, H., Qvortrup, K., Nielsen, L B., Hla, T., Di Lorenzo, A., Christoffersen, C. Impaired endothelial barrier function in apolipoprotein M-deficient mice is dependent on sphingosine-1-phosphate receptor 1.

OriginalsprogEngelsk
TidsskriftFASEB Journal
Vol/bind30
Udgave nummer6
Sider (fra-til)2351-9
Antal sider9
ISSN0892-6638
DOI
StatusUdgivet - jun. 2016

ID: 49289567