Postnatal Deletion of the Type II Transforming Growth Factor-β Receptor in Smooth Muscle Cells Causes Severe Aortopathy in Mice
Author(s) -
Jie Hu,
Wei Hao,
Mia Jaffe,
Nathan Airhart,
Liang Du,
Stoyan N. Angelov,
James Yan,
Julie K. Allen,
Inkyung Kang,
Thomas N. Wight,
Kate Fox,
Alexandra Smith,
Rachel Enstrom,
David A. Dichek
Publication year - 2015
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.115.306573
Subject(s) - biology , receptor , transforming growth factor beta , transforming growth factor , allele , microbiology and biotechnology , cancer research , gene , genetics
Prenatal deletion of the type II transforming growth factor-β (TGF-β) receptor (TBRII) prevents normal vascular morphogenesis and smooth muscle cell (SMC) differentiation, causing embryonic death. The role of TBRII in adult SMC is less well studied. Clarification of this role has important clinical implications because TBRII deletion should ablate TGF-β signaling, and blockade of TGF-β signaling is envisioned as a treatment for human aortopathies. We hypothesized that postnatal loss of SMC TBRII would cause aortopathy.
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