Abstract:A metalloprotease, ADAM17, mediates EGF receptor (EGFR) activation in vascular smooth muscle cells (VSMC) by angiotensin II (Ang II) leading to hypertrophy. dnADAM17 prevents vascular neointimal hyperplasia. To test if vascular ADAM17 silencing has any therapeutic potential against hypertension, we evaluated Ang II-induced end-organ damage as well as hypertension in ADAM17 flox/flox mice bred with sm22α Cre mice (Cre+/-). Upon Ang II infusion (1 μg/kg/min) for 2 weeks, control Cre-/- mice showed phenotypes of … Show more
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