MicroRNA-21 is a downstream effector of AKT that mediates its antiapoptotic effects via suppression of Fas ligand.

MicroRNA-21 (miR-21) is highly up-regulated during hypertrophic and cancerous cell growth. In contrast, we found that it declines in cardiac myocytes upon exposure to hypoxia. Thus, the objective was to explore its role during hypoxia.

An antagonism between the AKT and beta-adrenergic signaling pathways mediated through their reciprocal effects on miR-199a-5p.

We have recently reported that downregulation of miR-199a-5p is necessary and sufficient for inducing upregulation of its targets, including hypoxia-inducible factor-1 alpha (Hif-1 alpha) and Sirt1, during hypoxia preconditioning (HPC). Conversely, others and we have reported that miR-199a-5p is upregulated during cardiac hypertrophy. Thus, the objective of this study was to delineate the signaling pathways that regulate the expression of miR-199a-5p and its targets, and their role in myocyte survival during hypoxia.

Downregulation of miR-199a derepresses hypoxia-inducible factor-1alpha and Sirtuin 1 and recapitulates hypoxia preconditioning in cardiac myocytes.

MicroRNAs are posttranscriptional gene regulators that are differentially expressed during various diseases and have been implicated in the underlying pathogenesis. We report here that miR-199a is acutely downregulated in cardiac myocytes on a decline in oxygen tension. This reduction is required for the rapid upregulation of its target, hypoxia-inducible factor (Hif)-1alpha.

MicroRNAs challenge the status quo of therapeutic targeting.

MicroRNAs (miRNAs) are recently discovered posttranscriptional regulators of gene expression that have become a cause célèbre. There are currently more than 600 miRNAs identified in humans that are estimated to regulate about one third of all messenger RNA (mRNA). Because miRNA levels were found widely deregulated in diseases, they have been implicated in the underlying pathogenesis.

MicroRNA-21 targets Sprouty2 and promotes cellular outgrowths.

The posttranscriptional regulator, microRNA-21 (miR-21), is up-regulated in many forms of cancer, as well as during cardiac hypertrophic growth. To understand its role, we overexpressed it in cardiocytes where it revealed a unique type of cell-to-cell "linker" in the form of long slender outgrowths and branches. We subsequently confirmed that miR-21 directly targets and down-regulates the expression of Sprouty2 (SPRY2), an inhibitor of branching morphogenesis and neurite outgrowths.

MicroRNA with a MacroFunction.

With the advent of microRNA (miRNA) we are compelled to revise our understanding of the mechanisms underlying gene regulation during health and disease. A miRNA is approximately 21 ribonucleotides-long, genetically encoded, with a potential to recognize multiple mRNA targets guided by sequence complementarity and RNA-binding proteins. This class of molecules is functionally versatile, with the capacity to specifically inhibit translation initiation or elongation, as well as, induce mRNA degradation, through predominantly targeting the 3'-untranslated regions of mRNA.