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See related article, pages 880–893The human genome is replete with digital information, only 1.2% of which comprises protein-coding sequence. The nonprotein-coding sequence encompasses >1 million regulatory elements controlling gene expression and codes for such genomic processes as recombination, replication, splicing, transposition, and structural integration of the genome with the surrounding nucleoskeleton. Throughout such punctuated sequence information is a vast amount of transcribed nonprotein-coding RNA whose functions have only begun to be understood. These facts debunk the old notion that our genome is comprised largely of “junk DNA” and point to an ever-expanding role for genomic DNA sequence in various biological processes. For example, a portion of the nonprotein-coding RNA transcriptome encodes some 1000 microRNAs (miRs) whose activity relates primarily to the posttranscriptional regulation of the mRNA pool of a cell through targeted mRNA degradation.1 Accordingly, miRs function to influence essentially all aspects of cellular biology by tailoring the proteome of a cell. Since the initial reporting of miRs in human cells,2 there has been an explosive increase in the number of PubMed articles (Figure 1) related to these “molecular rheostats,” and there are high hopes for applying knowledge gained through this body of work in the treatment of numerous diseases in which aberrant expression of miRs has been reported across body systems.3Figure 1. Number of articles published on microRNAs over the past 11 years. The white bar represents the predicted number of additional articles to be published in 2011.Various cells of the cardiovascular system express a number of miRs that have been the subject of intense study over the past few years. These include the bicistronic miR1/133a and miR143/145 genes that are highly specific to cardiac myocytes and smooth muscle cells (SMC), respectively.4 The miR1/133a gene is of particular interest because it is duplicated on …

MicroRNA133a: A New Variable in Vascular Smooth Muscle Cell Phenotypic Switching