کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5506260 | 1400289 | 2017 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Activation of PPARγ does not contribute to macrophage ABCA1 expression and ABCA1-mediated cholesterol efflux to apoAI
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کلمات کلیدی
HDLPPARγABCA1CD36LXRhigh-density lipoprotein - HDL یا لیپوپروتئین با دانسیته بالا یا چگالی بالاTZDs - TZD هاthiazolidinediones - تیازولیدیدونهاCholesterol efflux - خروجی کلسترولMacrophages - ماکروفاژها،درشت خوارهاliver X receptor - کبد X گیرندهperoxisome proliferator-activated receptor γ - گیرنده پروتئین کننده پروکسیوم فعال γ
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Activation of macrophage ABCA1/G1 expression and cholesterol efflux is believed one of the mechanisms by which PPARγ inhibits atherosclerosis. PPARγ can also activate CD36 expression, a receptor for oxLDL, which may supply LXR ligands to activate LXR-ABCA1/G1 pathways. However, the controversial effects of PPARγ on ABCA1 expression have been reported. In this study, we used peritoneal macrophages isolated from wild type and CD36 deficient (CD36â/â) mice to clarify if PPARγ ligands can influence ABCA1 expression by CD36 function. We found that CD36 deficiency had no effect on cholesterol efflux and ABCA1/ABCG1 expression at basal levels. In both cell types, PPARγ ligands (15d-PGJ2, troglitazone and pioglitazone) reduced ABCA1 expression and ABCA1-mediated cholesterol efflux to apoAI, with most by troglitazone. LXR ligand-induced ABCA1 expression and cholesterol efflux was attenuated by PPARγ ligands. Associated with decreased ABCA1 protein levels, ABCA1 mRNA and promoter activity were reduced by PPARγ ligands. Furthermore, high expressing PPARγ reduced ABCA1 expression and LXR-activated ABCA1 promoter in a CD36-independent manner. In contrast, ABCG1 expression was induced by PPARγ ligands while inhibited by PPARγ inactivation. Taken together, our study suggests that enhancement of macrophage cholesterol metabolism by PPARγ is not contributed by activating ABCA1 expression and ABCA1-mediated cholesterol efflux to apoAI, which is not involved by CD36 expression either.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 482, Issue 4, 22 January 2017, Pages 849-856
Journal: Biochemical and Biophysical Research Communications - Volume 482, Issue 4, 22 January 2017, Pages 849-856
نویسندگان
Meixiu Jiang, Xiaoju Li,