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A role for Smad6 in development and homeostasis of the cardiovascular system
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A role for Smad6 in development and homeostasis of the cardiovascular system
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Journal Article
A role for Smad6 in development and homeostasis of the cardiovascular system
2000
Overview
Smad proteins are intracellular mediators of signalling initiated by Tgf-βsuperfamily ligands (Tgf-βs, activins and bone morphogenetic proteins (Bmps)). Smads 1, 2, 3, 5 and 8 are activated upon phosphorylation by specific type I receptors, and associate with the common partner Smad4 to trigger transcriptional responses
1
. The inhibitory Smads (6 and 7) are transcriptionally induced in cultured cells treated with Tgf-β superfamily ligands, and downregulate signalling in
in vitro
assays
2
,
3
,
4
,
5
,
6
,
7
. Gene disruption in mice has begun to reveal specific developmental and physiological functions of the signal-transducing Smads. Here we explore the role of an inhibitory Smad
in vivo
by targeted mutation of
Madh6
(which encodes the Smad6 protein). Targeted insertion of a
LacZ
reporter demonstrated that Smad6 expression is largely restricted to the heart and blood vessels, and that
Madh6
mutants have multiple cardiovascular abnormalities. Hyperplasia of the cardiac valves and outflow tract septation defects indicate a function for Smad6 in the regulation of endocardial cushion transformation. The role of Smad6 in the homeostasis of the adult cardiovascular system is indicated by the development of aortic ossification and elevated blood pressure in viable mutants. These defects highlight the importance of Smad6 in the tissue-specific modulation of Tgf-β superfamily signalling pathways
in vivo
.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animal Genetics and Genomics
/ Animals
/ Biological and medical sciences
/ Biomedical and Life Sciences
/ Cardiovascular Abnormalities - genetics
/ Cardiovascular System - embryology
/ Cardiovascular System - growth & development
/ Cell differentiation, maturation, development, hematopoiesis
/ Cloning
/ DNA-Binding Proteins - deficiency
/ DNA-Binding Proteins - genetics
/ DNA-Binding Proteins - metabolism
/ Embryos
/ Female
/ Fundamental and applied biological sciences. Psychology
/ Heart
/ letter
/ Ligands
/ Male
/ Mice
/ Molecular and cellular biology
/ Muscle, Smooth, Vascular - pathology
/ Muscle, Smooth, Vascular - physiology
/ Mutants
/ Mutation
/ Proteins
/ Recombinant Fusion Proteins - metabolism
/ Signal Transduction - physiology
