Adam10 is essential for early embryonic cardiovascular development.

Published

Journal Article

Notch pathway has been demonstrated to regulate cardiovascular development. One important step in Notch pathway is the cleavage of Notch receptor, during which an intracellular fragment of Notch protein is released to activate downstream genes. It is still uncertain whether Adam10, the mammalian homologue of Kuzbanian in Drosophila, is required to activate the Notch pathway during cardiovascular development. To further understand the physiological function of Adam10 in vascular and cardiac development, we generated mice lacking the Adam10 gene primarily in the endothelial compartment. We found that disruption of Adam10 in endothelial cells resulted in embryonic death after embryonic day 10.5 due to multiple cardiac and vascular defects similar to Notch1 mutants. We further showed that the expression of Notch target genes Snail and Bmp2 are impaired in Adam10-deficient cardiac tissues. Finally, we provide experimental evidence to support that Adam10 functions in a cell autonomous manner during mammalian cardiac development.

Full Text

Duke Authors

Cited Authors

  • Zhang, C; Tian, L; Chi, C; Wu, X; Yang, X; Han, M; Xu, T; Zhuang, Y; Deng, K

Published Date

  • October 2010

Published In

Volume / Issue

  • 239 / 10

Start / End Page

  • 2594 - 2602

PubMed ID

  • 20803506

Pubmed Central ID

  • 20803506

Electronic International Standard Serial Number (EISSN)

  • 1097-0177

Digital Object Identifier (DOI)

  • 10.1002/dvdy.22391

Language

  • eng

Conference Location

  • United States