Human SM22α BAC encompasses regulatory sequences for expression in vascular and visceral smooth muscles at fetal and adult stages

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Abstract
TheSM22α gene has widely been used to study the regulatory mechanisms of smooth muscle cell (SMC) gene expression during cardiovascular development. To determine the regulatory mechanisms for the evolutionarily conserved human SM22α (hSM22α) gene, we demonstrated that 445 bp upstream DNA sequences of hSM22α gene exhibited a high transcriptional activity in arterial SMC, not in venous nor in visceral SMCs during embryogensis. However, this promoter was gradually turned off in adulthood. Inclusion of the first intron in this promoter suppressed the promoter activity in pulmonary trunk arterial SMCs, whereas the expression in other systemic vasculature remained similar to that of the hSM22-445 promoter during the fetal and adult stages. To determine whether additional sequences are required forSM22α expression in all subtypes of SMCs, we examined the expression of a bacterial artificial chromosome containing the hSM22α locus in transgenic mice. The hSM22α transgene showed similar developmental expression patterns as the endogenous mouse SM22α gene, suggesting that this bacterial artificial chromosome contains essential regulatory sequences for its expression in arterial, venous, and visceral tissues during development.