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Bhardwaj                                                                                                                                                                                       MicroRNAs in atopic dermatitis






























           Figure 3: Role of miR-146a in inflammation in atopic dermatitis (red arrows indicate inhibitory effect). AD: atopic dermatitis; IFN-g:
           interferon-g; IL-4: interleukin-4; NF-kB: nuclear factor kappa B


           pathways. CCL5 and CCL8 are known to attract T     was upregulated in serum but was markedly decreased
           cells, macrophages and eosinophils [46,47] . Figure 3   in urine of children with AD [50] . Patients with higher
           summarizes the above information on role of miR-   IgE levels in serum had significantly lower expression
           146a in skin inflammation. Considering the important   of miR-203 in urine, but higher expression in serum
           role of miR-146a in suppression of innate immune   compared to controls. This contrary phenotype of miR-
           responses in keratinocytes, its overexpression may   203 could due to its expression from other organs
           have a potential role in treatment of AD and other   such as the esophagus. MiR-203 has previously
           inflammatory skin conditions. The success of TNFα   been identified as a keratinocyte-specific miRNA
           blockers in treatment of psoriasis leads us to believe   overexpressed in psoriasis [26] . Serum levels of miR-
           that miR-146a could be a novel therapeutic target   205 have been found to be significantly lower among
           as well.                                           patients with lupus compared to controls, and are
                                                              thought to positively correlate with renal function [49] .
           MIRNAS IN SERUM AND URINE                          It was, moreover, demonstrated that upregulated
                                                              miR-203 in serum was significantly associated with
                                                              expression of sTNFRI and sTNFRII. However, neither
           MiRNAs have been found in serum and plasma,        sTNFRI nor sTNFRII were shown to be the direct
           urine, tears and amniotic fluid making them promising   downstream targets of miR-203.
           biomarkers for various diseases [48,49] . Lv et al. [50]
           performed a genome-wide miRNA profiling in serum   Sonkoly et al. [26]  have also described a specific miRNA
           and urine of children with AD. The study confirmed   expression profile for psoriasis. They performed
           stable expression of miRNAs in serum and urine. Ten   a comprehensive analysis of all human miRNAs
           serum miRNAs and 17 urinary miRNAs were identified   registered in mirBase 8.0 in skin lesions of patients
           as significantly differentially expressed between   with psoriasis and compared it to expression in healthy
           children with AD and controls. MiR-483-5p and miR-  skin and lesional skin of patients with AD. Increased
           205 were upregulated in both serum and urine in    psoriasis-specific overexpression of miR-203 and
           children with AD compared to controls. Patients with   miR-146 was detected. MiR-21 was significantly
           higher IgE levels had significantly higher expression   upregulated in both psoriasis and AD, compared
           of miR-203 and miR-483-5p in serum compared        to healthy skin. A target of miR-203 is suppressor
           to controls. MiR-483-5p in serum was found to be   of cytokine signaling (SOCS-3) which has a role in
           significantly associated with other atopic conditions   inflammatory responses and keratinocyte functions.
           such as rhinitis and/or asthma, reflecting the multi-  The upregulation of miR-203 was found to be
           organ/tissue involvement of atopic conditions. MiR-203   associated with down-regulation of SOCS-3 [26] . On the


                           Journal of Translational Genetics and Genomics ¦ Volume 1 ¦ November 17, 2017   19
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