Demonstrates a transactivation mechanism where Angiotensin II utilizes EGFR as a bridge between a Gq-coupled receptor and phosphotyrosine generation to stimulate vascular smooth muscle cell growth.
Maps Ang II-EGFR transactivation in VSMCs; hypothesis-generating for targeted therapies in vascular remodeling.
The mechanism by which Ang II stimulates the growth of vascular smooth muscle cells was investigated by measuring the phosphorylation of mitogen-activated protein kinases ERK 1 and ERK 2. Ca2+ ionophore was found to have effects practically analogous to Ang II. We found that the signaling pathway involves the activation of epidermal growth factor receptor (EGFR) kinase, activation of the adaptor proteins Shc and Grb2, and the small G-protein Ras. Although the mechanism of AT1- (or Ca2+)-induced activation of EGFR is not yet clear, we have found that calcium-dependent protein kinase CAKss/PYK2 and c-Src are involved in this process. These studies indicate a transactivation mechanism that utilizes EGFR as a bridge between a Gq-coupled receptor and activation of phosphotyrosine generation.
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Inagami et al. (2000) studied this question.
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