Fibroblast growth factor plays a critical role in SM22alpha expression during Xenopus embryogenesis

Although 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 SM22alpha (XSM22alpha) as an SMC-specific marker. XSM22alpha cDNA contained a 600-bp open reading frame, and the predicted amino acid sequences were highly conserved in evolution. XSM22alpha 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, XSM22alpha transcripts were restricted to the vascular and visceral SMCs. XSM22alpha 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 XSM22alpha expression. These results suggest that XSM22alpha is a useful molecular marker for the SMC lineage in Xenopus and that FGF signaling plays an important role in the induction of XSM22alpha and in the differentiation of SMCs.