Abstract P143: Hypertension and Inflammation-Related microRNAs

microRNAs (miRs) are short single stranded noncoding RNAs that are involved in the regulation of a number of physiological and pathological processes. miRs down regulate target gene expression post-transcriptionally by degrading messenger RNA and/or by blocking translation. It is now recognized that miRs play a key role in regulating inflammation, vascular health and in-turn, cardiovascular disease (CVD). For example, altered expression of specific miRs such as, miR-126, miR-146a and miR-150 have been linked with heightened vascular inflammation and CVD risk. Hypertension is associated with increased inflammatory burden. The mechanisms underlying blood pressure-related inflammatory stress are not fully understood. It is currently unknown whether inflammation-related miRs are dysregulated with elevated blood pressure. Accordingly, the aim of this ongoing study is to determine the influence of hypertension, independent of other risk factors, on circulating expression of miR-34a, miR-92a, miR -126, miR-146a and miR-150. To date, 28 sedentary, middle-aged adults have been studied: 14 normotensive (NT; 12M/2F; age: 53±1 yr; BP: 114/71±2/1 mmHg) and 14 hypertensive (HT; 12M/2F; 56±2 yr; 142/90±2/2 mmHg). All subjects were non-smokers, normolipidemic, non-medicated and free of overt CVD. Circulating expression of miRs was determined in plasma using standard RT-PCR techniques with miR primers of interest. Expression was normalized to exogenous C. elegans miR-39 and reported as relative expression in arbitrary units (AU). Circulating expression of miR-126 (0.14±0.03 vs 0.33±0.04 AU) and miR-150 (0.06±0.02 vs 0.12±0.02 AU) were markedly lower (~135% and 100%, respectively; P<0.05) in the HT vs NT groups. There was no significant group difference in miR-34a (0.017±0.005 vs 0.010±0.001 AU), miR-92a (0.66±0.16 vs 1.01±0.13 AU) and miR-146a (0.04±0.01 vs 0.06±0.01 AU). Lower expression of miR-126 and miR-150 is consistent with a proinflammatory phenotype, as both are involved in limiting inflammatory pathways. In summary, these initial results suggest that dysregulation of key inflammation-related miRs may contribute mechanistically to the heightened inflammatory state associated with elevated blood pressure and deserve further study.