These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: PPARgamma1-induced caveolin-1 enhances cholesterol efflux and attenuates atherosclerosis in apolipoprotein E-deficient mice.
    Author: Hu Q, Zhang XJ, Liu CX, Wang XP, Zhang Y.
    Journal: J Vasc Res; 2010; 47(1):69-79. PubMed ID: 19729954.
    Abstract:
    OBJECTIVE: Caveolin-1 (Cav-1) may positively or negatively influence the development of atherosclerosis, depending on the cell type and the metabolic pathways regulated by this protein. We investigate the effects of Cav-1 on cholesterol efflux in RAW264.7 infected with AdPPARgamma1 and whether Cav-1 could attenuate established atherosclerotic lesions in PPARgamma1-treated apoE-deficient mice. METHODS AND RESULTS: Compared with AdGFP control, PPARgamma1 and Cav-1 were constitutively overexpressed in AdPPARgamma1-infected RAW264.7 cells, which stimulated cholesterol efflux to apolipoprotein A-I. Using a small interfering RNA approach (Cav-1-siRNA) we achieved an efficient and specific knockdown of caveolin-1 expression (80%), which resulted in a remarkable reduction of cholesterol efflux in RAW264.7 cells . Moreover, PPARgamma1-treated Cav-1-siRNA RAW264.7 cells showed more ability to stimulate cholesterol efflux than Cav-1-siRNA RAW264.7 cells, but far less than control-siRNA RAW264.7 cells and PPARgamma1-treated RAW264.7 cells. In addition, 40-week-old apoE-deficient mice fed a Western-type diet and infected for 4 weeks with AdPPARgamma1 showed induced Cav-1 expression in aortic vascular endothelial cells, smooth muscle cells and macrophages, as well as attenuated established atherosclerotic lesions. CONCLUSIONS: PPARgamma1 gene therapy could induce Cav-1 expression and enhance cholesterol efflux and attenuate atherosclerosis in apoE-deficient mice.
    [Abstract] [Full Text] [Related] [New Search]