Skip to main content
placeholder image

Visfatin Destabilizes Atherosclerotic Plaques in Apolipoprotein E-Deficient Mice.

Journal Article


Abstract


  • Objectives

    Although there is evidence that visfatin is associated with atherogenesis, the effect of visfatin on plaque stability has not yet been explored.

    Methods

    In vivo, vulnerable plaques were established by carotid collar placement in apolipoprotein E-deficient (ApoE-/-) mice, and lentivirus expressing visfatin (lenti-visfatin) was locally infused in the carotid artery. The lipid, macrophage, smooth muscle cell (SMC) and collagen levels were evaluated, and the vulnerability index was calculated. In vitro, RAW264.7 cells were stimulated with visfatin, and the MMPs expressions were assessed by western blot and immunofluorescence. And the mechanism that involved in visfatin-induced MMP-8 production was investigated.

    Results

    Transfection with lenti-visfatin significantly promoted the expression of visfatin which mainly expressed in macrophages in the plaque. Lenti-visfatin transfection significantly promoted the accumulation of lipids and macrophages, modulated the phenotypes of smooth muscle cells and decreased the collagen levels in the plaques, which significantly decreased the plaque stability. Simultaneously, transfection with lenti-visfatin significantly up-regulated the expression of MMP-8 in vivo, as well as MMP-1, MMP-2 and MMP-9. Recombinant visfatin dose- and time-dependently up-regulated the in vitro expression of MMP-8 in macrophages. Visfatin promoted the translocation of NF-κB, and inhibition of NF-κB significantly reduced visfatin-induced MMP-8 production.

    Conclusions

    Visfatin increased MMP-8 expression, promoted collagen degradation and increased the plaques vulnerability index.

Publication Date


  • 2016

Citation


  • Li, B., Zhao, Y., Liu, H., Meng, B., Wang, J., Qi, T., . . . An, F. (2016). Visfatin Destabilizes Atherosclerotic Plaques in Apolipoprotein E-Deficient Mice.. PloS one, 11(2), e0148273. doi:10.1371/journal.pone.0148273

Web Of Science Accession Number


Start Page


  • e0148273

Volume


  • 11

Issue


  • 2

Abstract


  • Objectives

    Although there is evidence that visfatin is associated with atherogenesis, the effect of visfatin on plaque stability has not yet been explored.

    Methods

    In vivo, vulnerable plaques were established by carotid collar placement in apolipoprotein E-deficient (ApoE-/-) mice, and lentivirus expressing visfatin (lenti-visfatin) was locally infused in the carotid artery. The lipid, macrophage, smooth muscle cell (SMC) and collagen levels were evaluated, and the vulnerability index was calculated. In vitro, RAW264.7 cells were stimulated with visfatin, and the MMPs expressions were assessed by western blot and immunofluorescence. And the mechanism that involved in visfatin-induced MMP-8 production was investigated.

    Results

    Transfection with lenti-visfatin significantly promoted the expression of visfatin which mainly expressed in macrophages in the plaque. Lenti-visfatin transfection significantly promoted the accumulation of lipids and macrophages, modulated the phenotypes of smooth muscle cells and decreased the collagen levels in the plaques, which significantly decreased the plaque stability. Simultaneously, transfection with lenti-visfatin significantly up-regulated the expression of MMP-8 in vivo, as well as MMP-1, MMP-2 and MMP-9. Recombinant visfatin dose- and time-dependently up-regulated the in vitro expression of MMP-8 in macrophages. Visfatin promoted the translocation of NF-κB, and inhibition of NF-κB significantly reduced visfatin-induced MMP-8 production.

    Conclusions

    Visfatin increased MMP-8 expression, promoted collagen degradation and increased the plaques vulnerability index.

Publication Date


  • 2016

Citation


  • Li, B., Zhao, Y., Liu, H., Meng, B., Wang, J., Qi, T., . . . An, F. (2016). Visfatin Destabilizes Atherosclerotic Plaques in Apolipoprotein E-Deficient Mice.. PloS one, 11(2), e0148273. doi:10.1371/journal.pone.0148273

Web Of Science Accession Number


Start Page


  • e0148273

Volume


  • 11

Issue


  • 2