کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5942481 | 1574712 | 2016 | 4 صفحه PDF | دانلود رایگان |
- Endothelial-mesenchymal transitions (EndMTs) in atherosclerotic lesions contribute to calcification.
- Stem cell and mesenchymal markers, including Sox2, are upregulated in aortic endothelial cells (ECs) of fat-fed ApoEâ/â mice.
- Limiting Sox2 decreases the stem cell and mesenchymal markers and calcification in ApoE â/â aortas.
- A complex of serine proteases is upregulated in ApoE â/â aortic ECs.
- Blockade of these proteases reduces expression of Sox2 and atherosclerotic lesion calcification.
Background and aimsEndothelial-mesenchymal transitions (EndMTs) in endothelial cells (ECs) contribute to vascular disease.MethodsWe used ApoEâ/â mice fed a high-fat/high-cholesterol diet.ResultsWe reported evidence of EndMT in atherosclerotic lesions contributing to calcification. Stem cell and mesenchymal markers, including sex-determining region Y-box 2 (Sox2), were upregulated in aortic ECs of fat-fed ApoEâ/â mice. Limiting Sox2 decreased marker expression and calcification in ApoEâ/â aortas. Furthermore, a complex of serine proteases was upregulated in ApoEâ/â aortic ECs. Blockade of these proteases reduced expression of Sox2 and atherosclerotic lesion calcification.ConclusionsTogether, our data suggest that EndMTs contribute to atherosclerotic lesion calcification.
Journal: Atherosclerosis - Volume 253, October 2016, Pages 124-127