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Sökning: WFRF:(Nurmi E)

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  • Saliba-Gustafsson, P., et al. (författare)
  • Subclinical atherosclerosis and its progression are modulated by PLIN2 through a feed-forward loop between LXR and autophagy
  • 2019
  • Ingår i: Journal of Internal Medicine. - : Wiley-Blackwell. - 0954-6820 .- 1365-2796. ; 286:6, s. 660-675
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Hyperlipidaemia is a major risk factor for cardiovascular disease, and atherosclerosis is the underlying cause of both myocardial infarction and stroke. We have previously shown that the Pro251 variant of perilipin-2 reduces plasma triglycerides and may therefore be beneficial to reduce atherosclerosis development. Objective We sought to delineate putative beneficial effects of the Pro251 variant of perlipin-2 on subclinical atherosclerosis and the mechanism by which it acts. Methods A pan-European cohort of high-risk individuals where carotid intima-media thickness has been assessed was adopted. Human primary monocyte-derived macrophages were prepared from whole blood from individuals recruited by perilipin-2 genotype or from buffy coats from the Karolinska University hospital blood central. Results The Pro251 variant of perilipin-2 is associated with decreased intima-media thickness at baseline and over 30 months of follow-up. Using human primary monocyte-derived macrophages from carriers of the beneficial Pro251 variant, we show that this variant increases autophagy activity, cholesterol efflux and a controlled inflammatory response. Through extensive mechanistic studies, we demonstrate that increase in autophagy activity is accompanied with an increase in liver-X-receptor (LXR) activity and that LXR and autophagy reciprocally activate each other in a feed-forward loop, regulated by CYP27A1 and 27OH-cholesterol. Conclusions For the first time, we show that perilipin-2 affects susceptibility to human atherosclerosis through activation of autophagy and stimulation of cholesterol efflux. We demonstrate that perilipin-2 modulates levels of the LXR ligand 27OH-cholesterol and initiates a feed-forward loop where LXR and autophagy reciprocally activate each other; the mechanism by which perilipin-2 exerts its beneficial effects on subclinical atherosclerosis.
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  • Airiskallio, E., et al. (författare)
  • Third element effect in the surface zone of Fe-Cr-Al alloys
  • 2010
  • Ingår i: Physical Review B. Condensed Matter and Materials Physics. - 1098-0121 .- 1550-235X. ; 81:3
  • Tidskriftsartikel (refereegranskat)abstract
    • The third element effect to improve the high temperature corrosion resistance of the low-Al Fe-Cr-Al alloys is suggested to involve a mechanism that boosts the recovering of the Al concentration to the required level in the Al-depleted zone beneath the oxide layer. We propose that the key factor in this mechanism is the coexistent Cr depletion that helps to maintain a sufficient Al content in the depleted zone. Several previous experiments related to our study support that conditions for such a mechanism to be functional prevail in real oxidation processes of Fe-Cr-Al alloys.
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  • Airiskallio, E., et al. (författare)
  • Tuning the surface chemistry of Fe-Cr by V doping
  • 2009
  • Ingår i: Physical Review B. Condensed Matter and Materials Physics. - 1098-0121 .- 1550-235X. ; 80:15
  • Tidskriftsartikel (refereegranskat)abstract
    • The reversal of the magnitudes of the bulk and surface chemical-potential differences induces the outburst of Cr on the otherwise pure Fe surface of Fe-Cr alloys. This threshold value for the Cr content is about 10 at. %. It is found that vanadium addition to Fe-Cr shifts the Cr threshold to a substantially lower value suggesting V having a positive effect on the corrosion resistance of low Cr steels. The obtained shift in the Cr threshold is shown to be connected to the change in volume of the alloy.
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  • Resultat 1-10 av 48
  • [1]2345Nästa

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