Vascular Biology |
Expression During Xenopus Embryogenesis
From the Department of Cardiovascular Medicine, Graduate School of Medicine (T.O., I.S., K.M., S.K., Y.H., R.N., Y.Y., I.K.), the Laboratory of Molecular Embryology, Department of Biological Sciences, Graduate School of Science (K.S.), and the Department of Life Sciences (Biology), Graduate School of Arts and Sciences (M.A.), University of Tokyo, Tokyo, Japan.
Correspondence to Dr Issei Komuro, Department of Cardiovascular Medicine, University of Tokyo Graduate School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. E-mail komuro-tky{at}umin.ac.jp
AbstractAlthough smooth muscle
cells (SMCs) are critical components of the circulatory system, the
regulatory mechanisms of SMC differentiation remain largely unknown. In
the present study, we examined the mechanism of SMC differentiation
by using Xenopus laevis SM22
(XSM22
) as an
SMC-specific marker. XSM22
cDNA contained a 600-bp open reading
frame, and the predicted amino acid sequences were highly conserved in
evolution. XSM22
transcripts were first detected in heart anlage,
head mesenchyme, and the dorsal side of the lateral plate mesoderm at
the tail-bud stage, possibly representing the precursors of
muscle lineage. At the tadpole stage, XSM22
transcripts were
restricted to the vascular and visceral SMCs. XSM22
was strongly
induced by basic fibroblast growth factor (FGF) in animal caps.
Although expressions of Xenopus cardiac actin were not
affected by the expression of a dominant-negative FGF receptor, its
injection dramatically suppressed the XSM22
expression. These
results suggest that XSM22
is a useful molecular marker for the SMC
lineage in Xenopus and that FGF signaling plays an
important role in the induction of XSM22
and in the differentiation
of SMCs.
Key Words: smooth muscle cells SM22
basic fibroblast growth factor dominant-negative fibroblast growth factor receptor
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