2014
DOI: 10.1016/j.gene.2014.04.069
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miR-326 and miR-26a, two potential markers for diagnosis of relapse and remission phases in patient with relapsing–remitting multiple sclerosis

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Cited by 87 publications
(48 citation statements)
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“…For example, treatment with natalizumab resulted in differential expression of two clusters, miR‐17‐92 and miR‐106b‐25, in patients with MS, and affected CD4 + T‐cell activation and proliferation . Several microRNAs (such as miR‐326 and miR‐26a) have been reported to be associated with the pathogenesis of MS as a regulator of B‐cell, T‐cell and monocyte development . The precise role of microRNAs in the regulation of the pathogenesis of MS is not completely clear.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…For example, treatment with natalizumab resulted in differential expression of two clusters, miR‐17‐92 and miR‐106b‐25, in patients with MS, and affected CD4 + T‐cell activation and proliferation . Several microRNAs (such as miR‐326 and miR‐26a) have been reported to be associated with the pathogenesis of MS as a regulator of B‐cell, T‐cell and monocyte development . The precise role of microRNAs in the regulation of the pathogenesis of MS is not completely clear.…”
Section: Discussionmentioning
confidence: 99%
“…[34][35][36] Several micro-RNAs (such as miR-326 and miR-26a) have been reported to be associated with the pathogenesis of MS as a regulator of B-cell, T-cell and monocyte development. 23,37 The precise role of microRNAs in the regulation of the pathogenesis of MS is not completely clear. miR-326 and miR-26a were reported to regulate Th17 cell differentiation in MS. miR-155 and let-7e were reported to regulate Th1 cell differentiation in a mouse model of MS. 24,25,32 The miR-132-Surtuin-1 axis was reported to regulate B-cell cytokine production in MS. 38 Our study demonstrates for the first time that miR-140-5p could be a Th1 regulator, and therefore is associated with the pathogenesis of MS. miR-140-5p was originally found in cartilage.…”
Section: Discussionmentioning
confidence: 99%
“…It has been reported that M‐MDSC acquires phenotypic, morphological, and functional features from PMN‐MDSC by a mechanism that histone deacetylase 2 (HDAC2) binds to the retinoblastoma protein (Rb1) promoter region, resulting in down‐regulation of Rb1 expression in the tumor microenvironment . The generation, proliferation, migration, and immunosuppressive effects of MDSCs are regulated by various cytokines through multiple pathways, such as IL‐4, IL‐6, IL‐10, and IL‐13, which are mainly involved in the regulation of the generation and activation of MDSCs, promoting the proliferation and enhancing the immunosuppression function of MDSCs . The cyclooxygenase 2 (COX2)/prostaglandin E2 (PGE2) pathway also affects the generation and proliferation of MDSCs, thereby inhibiting the function of T cells.…”
Section: Characteristic Phenotypes Of Mdscsmentioning
confidence: 99%
“…miRNA profiling has also been suggested for use in identifying biomarkers of MS and revealing new methods for diagnosing patients. miR-326 and miR-26a have emerged as potential biomarkers for discriminating between relapsing and remitting MS (Honardoost et al, 2014).…”
Section: Mirna's and Myelin Diseasementioning
confidence: 99%