Na-H exchanger 1 determines atherosclerotic lesion acidification and promotes atherogenesis.

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ID: 43606
2019
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Abstract
The pH in atherosclerotic lesions varies between individuals. IgE activates macrophage Na-H exchanger (Nhe1) and induces extracellular acidification and cell apoptosis. Here, we show that the pH-sensitive pHrodo probe localizes the acidic regions in atherosclerotic lesions to macrophages, IgE, and cell apoptosis. In Apoe mice, Nhe1-deficiency or anti-IgE antibody reduces atherosclerosis and blocks lesion acidification. Reduced atherosclerosis in Apoe mice receiving bone marrow from Nhe1- or IgE receptor FcεR1-deficient mice, blunted foam cell formation and signaling in IgE-activated macrophages from Nhe1-deficient mice, immunocomplex formation of Nhe1 and FcεR1 in IgE-activated macrophages, and Nhe1-FcεR1 colocalization in atherosclerotic lesion macrophages support a role of IgE-mediated macrophage Nhe1 activation in atherosclerosis. Intravenous administration of a near-infrared fluorescent pH-sensitive probe LS662, followed by coregistered fluorescent molecular tomography-computed tomography imaging, identifies acidic regions in atherosclerotic lesions in live mice, ushering a non-invasive and radiation-free imaging approach to monitor atherosclerotic lesions in live subjects.
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liu2019nahnature Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Liu, Cong-Lin;Zhang, Xian;Liu, Jing;Wang, Yunzhe;Sukhova, Galina K;Wojtkiewicz, Gregory R;Liu, Tianxiao;Tang, Rui;Achilefu, Samuel;Nahrendorf, Matthias;Libby, Peter;Guo, Junli;Zhang, Jin-Ying;Shi, Guo-Ping;
Journal Nature communications
Year 2019
DOI
10.1038/s41467-019-11983-3
URL
Keywords
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