TY - JOUR
T1 - Adamts18 modulates the development of the aortic arch and common carotid artery
AU - Ye, Shuai
AU - Yang, Ning
AU - Lu, Tiantian
AU - Wu, Taojing
AU - Wang, Liya
AU - Pan, Yi Hsuan
AU - Cao, Xiaohua
AU - Yuan, Xiaobing
AU - Wisniewski, Thomas
AU - Dang, Suying
AU - Zhang, Wei
N1 - Publisher Copyright:
© 2021 The Authors
PY - 2021/6/25
Y1 - 2021/6/25
N2 - Members of a disintegrin and metalloproteinases with thrombospondin motif (ADAMTS) family have been implicated in various vascular diseases. However, their functional roles in early embryonic vascular development are unknown. In this study, we showed that Adamts18 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.
AB - Members of a disintegrin and metalloproteinases with thrombospondin motif (ADAMTS) family have been implicated in various vascular diseases. However, their functional roles in early embryonic vascular development are unknown. In this study, we showed that Adamts18 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.
KW - cell biology
KW - developmental biology
UR - https://www.scopus.com/pages/publications/85107762320
U2 - 10.1016/j.isci.2021.102672
DO - 10.1016/j.isci.2021.102672
M3 - 文章
AN - SCOPUS:85107762320
SN - 2589-0042
VL - 24
JO - iScience
JF - iScience
IS - 6
M1 - 102672
ER -