Absence of TGFβ signaling in embryonic vascular smooth muscle leads to reduced lysyl oxidase expression, impaired elastogenesis, and aneurysm
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Abstract
Abstract To address the requirement for TGFβ signaling in the formation and maintenance of the vascular matrix, we employed lineage‐specific mutation of the type II TGFβ receptor gene ( Tgfbr2 ) in vascular smooth muscle precursors in mice. In both neural crest‐ and mesoderm‐derived smooth muscle, absence of TGFβ receptor function resulted in a poorly organized vascular elastic matrix in late‐stage embryos which was prone to dilation and aneurysm. This defect represents a failure to initiate formation of the elastic matrix, rather than a failure to maintain a preexisting matrix. In mutant tissue, lysyl oxidase expression was substantially reduced, which may contribute to the observed pathology. genesis 47:115–121, 2009. © 2009 Wiley‐Liss, Inc.
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