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Acta Physiologica Congress

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Acta Physiologica 2012; Volume 204, Supplement 689
91st Annual Meeting of The German Physiological Society
3/22/2012-3/25/2012
Dresden, Germany


INVESTIGATION OF STEROID RECEPTOR-DEPENDENT MIRNA ALTERATIONS IN PRIMARY HUMAN ENDOTHELIAL AND VASCULAR SMOOTH MUSCLE CELLS
Abstract number: P047

Bretschneider1 *M., Grossmann1 C., Gekle1 M.

1J.-B.-Institut fr Physiologie/ MLU, Medicine, Halle, Germany

MicroRNAs (miRNAs) have a widespread impact on e.g. cell growth, differentiation and development, by acting as posttranscriptional modulators of gene expression. Little is known about these small, non-coding RNA molecules in reference to mineralocorticoid (MR) and glucocorticoid receptor (GR) actions in the cardiovascular system and in general. While the MR influences electrolyte homeostasis and blood pressure, the GR is important for inflammation, metabolism and development. In contrast to their different functions, both steroid receptors act as transcription factors at the same hormone response element. Some pathophysiological effects in the vasculature, which are mediated by MR, but not GR, might be controlled by miRNA actions. To test this hypothesis we analyzed the miRNA expression levels in human aortic endothelial (HAoECs) and human aortic smooth muscle cells (HAoSMCs) before and after incubation with aldosterone (MR ligand) or dexamethasone (MR/GR ligand). The obtained data were confirmed with TaqMan qPCR. Our results showed miR-449c* and miR-29b to be the most significantly altered miRNAs. The expression level of miR-449c* is upregulated in HAoECs after stimulation with aldosterone or dexamethasone and decreased in HAoSMCs under both conditions, giving an interesting approach for potential regulatory functions. Downregulation of miR-29b was detected in HAoSMCs, after aldosterone or dexamethasone incubation. Upcoming analysis via in silico prediction and reporter gene assays will reveal potential targets of these miRNAs, with the goal to elucidate the mechanism of MR and GR effects in cardiovascular biology and disease.

To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 204, Supplement 689 :P047

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