Boström Kristina I, Yao Jiayi, Guihard Pierre J, Blazquez-Medela Ana M, Yao Yucheng
Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA; The Molecular Biology Institute at UCLA, Los Angeles, CA 90095-1570, USA.
Division of Cardiology, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA.
Atherosclerosis. 2016 Oct;253:124-127. doi: 10.1016/j.atherosclerosis.2016.08.046. Epub 2016 Sep 2.
Endothelial-mesenchymal transitions (EndMTs) in endothelial cells (ECs) contribute to vascular disease.
We used ApoE mice fed a high-fat/high-cholesterol diet.
We 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 ApoE mice. Limiting Sox2 decreased marker expression and calcification in ApoE aortas. Furthermore, a complex of serine proteases was upregulated in ApoE aortic ECs. Blockade of these proteases reduced expression of Sox2 and atherosclerotic lesion calcification.
Together, our data suggest that EndMTs contribute to atherosclerotic lesion calcification.
内皮细胞中的内皮-间充质转化（EndMTs）会导致血管疾病。
我们使用喂食高脂/高胆固醇饮食的载脂蛋白E（ApoE）小鼠。
我们报告了在促成钙化的动脉粥样硬化病变中存在EndMT的证据。包括性别决定区Y盒2（Sox2）在内的干细胞和间充质标志物在喂食脂肪的ApoE小鼠的主动脉内皮细胞中上调。限制Sox2可降低ApoE主动脉中的标志物表达和钙化。此外，丝氨酸蛋白酶复合物在ApoE主动脉内皮细胞中上调。阻断这些蛋白酶可降低Sox2的表达和动脉粥样硬化病变钙化。
总之，我们的数据表明EndMTs促成动脉粥样硬化病变钙化。
