to understand the role of specific microRNAs as biomarkers for disease activity (DA) and progression. Our aim was to evaluate the peripheral blood (PB) expression of miR-155 in SLE patients and to determine its correlation with the DA in the clinical practice. Materials and methods We studied 40 SLE patients and 32 healthy controls. miR-155 expression levels in whole PB samples were determined by PCR (SYBR Green technology). 2-dd Ct method was used for analysis. The DA was assessed by SLE DA index (SLEDAI).Results miR-155 was upregulated in 50.0% of the patients and without difference in its expression levels in 17 (42.5%) of the patients. ROC curve analysis was conducted in order to evaluate the diagnostic accuracy of the PB expression levels of the studied miRNA. AUC for miR-155 was 0.691 (95% CI: 0.566 to 0.817), p=0.005 with 77.5% sensitivity and 50.0% specificity when the RQ cut value was 1.03. Levels of miR-155 correlated with the diagnosis (rs 0,330, p=0,005), with patient's age (rs 0,366, p=0,002) as well as with the presence of secondary Raynaud phenomenon (rs 0,250, p=0,035). There was no correlations with SLEDAI (p=0, 894) nor with the immunological activity according to ANA titer (p=0.399), a-dsDNA (p=0.817), a-Sm (p=0.285), a-b2GPI (p=0.903), a-CL antibodies (p=0.857) and C3 and C4 complement levels (p=0.062 and p=0.550, respectively). Conclusions We found a dysregulation of miR-155 in SLE which could suggests its role in the disease pathogenesis. There was no correlation between PB levels of miR-155 and DA as a whole as well as with the immunological activity which might reflect the variants of SLE DA in the studied patients, the difference in their genetic background or in the used medications but larger study is needed to confirm these results in the clinical practice.
Chronic progressive kidney disease (CKD) remains an unsolved problem in clinical Nephrology as neither biomarkers to predict progression towards end-stage renal failure in individual patients nor specific drugs to inhibit decline of kidney function are available in the clinic yet. In this regard, the prototypical epigenetic mechanism of CpG island promoter methylation has emerged as modulator of disease progression with utilities both as biomarker and as therapeutic target. Recent studies demonstrated the potential of hydralazine, a long-established antihypertensive drug with de-methylating activity, to reverse aberrant CpG island promoter aberration and ameliorate progression of chronic kidney disease. Here we review contribution of aberrant promoter methylation to progression of fibrogenesis and mechanisms underlying hydralazine's demethylating activity and discuss possible translational implications.Citation: Zeisberg EM, Zeisberg M (2016) Inhibition of Fibrogenesis upon Hydralazine-induced DNA Demethylation. J Kidney 2: 124.
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