Among various miRNA, miR-155 has been associated with the regulation of different immune-related processes, such as haematopoiesis,14 B-cell and T-cell differentiation,15 cancer16 and innate immunity.12 The miR-155 is processed from an exon of a non-coding RNA transcribed from the B-cell Integration Cluster located on chromosome 21, showing strong sequence homology BMN 673 ic50 among humans, mice and hens, and is highly expressed in cells of lymphoid and myeloid origin.17 Recently, miR-155 has been identified
and characterized as a component of macrophage and monocyte response to different types of inflammatory mediators, such as bacterial lipopolysaccharide (LPS), interferon-β (IFN-β), tumour necrosis factor-α (TNF-α) and polyriboinosinic-polyribocytidylic acid [poly(I:C)].12,18,19 Many of the miR-155 target transcripts identified so far are pro-apoptotic and anti-inflammatory proteins, such as the Fas-associated death domain protein, IκB kinase ε, inositol 5-phosphatase 1 and the suppressor of cytokine signalling-1 (SOCS-1). SOCS-1 belongs to a family Palbociclib mw of proteins known to regulate the response
of immune cells to cytokines and other inflammatory stimuli, such as LPS, through direct inhibition of the Janus tyrosine kinase (JAK) and consequent inhibition of signal transducer and activator of transcription factors (STAT), as a ‘classical’ negative feedback loop. In addition, the C-terminal SOCS box domain interacts with components of the ubiquitin ligase system and mediates proteasomal degradation of associated proteins, including key elements of other pro-inflammatory pathways, such as the nuclear
factor-κB and Jun N-terminal kinase pathways. Experimental evidence suggests that miR-155 plays a pro-inflammatory role and may be implicated in chronic inflammatory processes, such as those tuclazepam contributing to cancer and to certain neurodegenerative diseases. Given the similarities between microglia and other cells of the immune system, such as macrophages and dendritic cells, where miR-155 has been found to be up-regulated upon activation,20 in this work we investigated the contribution of miRNA-155 to microglia activation and microglia-mediated immune responses. To our knowledge, this is the first study providing evidence that miR-155 has a strong pro-inflammatory role during microglia activation and is required for SOCS-1 post-transcriptional regulation and progression of the immune response in these cells. Moreover, our results suggest that miR-155 inhibition induces neuronal protection from microglia-induced damage, and miR-155 may therefore constitute an interesting and promising target for the control of neuronal inflammation.
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