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Na+-H+ exchanger 1 determines atherosclerotic lesion acidification and promotes atherogenesis
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Journal Article
Na+-H+ exchanger 1 determines atherosclerotic lesion acidification and promotes atherogenesis
2019
Overview
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.
Na+-H+ exchanger 1 (Nhe1) regulates extracellular pH by extruding protons in exchange for extracellular Na+ . Here, Liu et al. show that Nhe1 promotes the development and acidification of atherosclerotic lesions and that pH-sensitive probes can be used to monitor plaque growth and acidification.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 14/34
/ 59/5
/ 64/60
/ Animals
/ Apolipoproteins E - deficiency
/ Apolipoproteins E - genetics
/ Atherosclerosis - metabolism
/ Humanities and Social Sciences
/ Humans
/ Hydrogen
/ Lesions
/ Macrophage Activation - genetics
/ Plaque, Atherosclerotic - genetics
/ Plaque, Atherosclerotic - metabolism
/ Science
/ Signal Transduction - genetics
