Key result
Treatment of R22 cultured rat aortic smooth muscle cells with monensin repressed tropoelastin gene expression at the mRNA level by approximately 50-fold.
Effect estimate: ca. 50-fold repression
Blockage of protein secretion by monensin represses tropoelastin synthesis at the mRNA level, suggesting autoregulation of tropoelastin gene expression.
Autoregulation of tropoelastin in smooth muscle cells extends molecular insights; leaves open in vivo relevance to vascular disease.
The blockage of protein secretion in the R22 cultured rat aortic smooth muscle cell strain with monensin repressed tropoelastin gene expression at the mRNA level by ca. 50-fold as measured by biosynthetic pulse-labeling, in vitro translation, and hybridization with a tropoelastin genomic DNA probe. These results suggest that tropoelastin gene expression is autoregulated, and they represent the first reported effect of monensin on gene expression.
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Frisch et al. (1985) studied this question. Monensin vs. Untreated cells was evaluated on Tropoelastin mRNA levels (ca. 50-fold repression). Treatment of R22 cultured rat aortic smooth muscle cells with monensin repressed tropoelastin gene expression at the mRNA level by approximately 50-fold.
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