Adamts18 modulates the development of the aortic arch and common carotid artery
Shuai Ye, Ning Yang, Tiantian Lu, Taojing Wu, Liya Wang, Yi-Hsuan Pan, Xiaohua Cao, Xiao‐bing Yuan, Thomas Wısnıewskı, Suying Dang, Wei Zhang
Abstract
is highly expressed at E11.5-E14.5 in cells surrounding the embryonic aortic arch (AOAR) and the common carotid artery (CCA) during branchial arch artery development in mice. Adamts18 deficiency was found to cause abnormal development of AOAR, CCA, and the third and fourth branchial arch appendages, leading to hypoplastic carotid body, thymus, and variation of middle cerebral artery. Adamts18 was shown to affect the accumulation of extracellular matrix (ECM) components, in particular fibronectin (Fn), around AOAR and CCA. As a result of increased Fn accumulation, the Notch3 signaling pathway was activated to promote the differentiation of cranial neural crest cells (CNCCs) to vascular smooth muscle cells. These data indicate that Adamts18-mediated ECM homeostasis is crucial for the differentiation of CNCCs.