- Open Access
Involvement of miR-126 in autoimmune disorders
© The Author(s) 2018
- Received: 8 December 2017
- Accepted: 3 April 2018
- Published: 2 May 2018
Micro-RNA represent a great family of small non-condign ribonucleic acid molecules; in particular microRNA-126 is an important member of this family and is expressed in many human cells such as cardiomyocytes, endothelial and lung cells. Some studies have shown the implication of miR-126 in cancer, but recently significant progresses have also been made in determining the role of miR-126 regulating immune-related diseases; probably, in a near future, they could potentially serve as diagnostic biomarkers or therapeutic targets.
The purpose of this review is to investigate the role of miR-126 in autoimmune diseases, so as to offer innovative therapies.
According literature, it was concluded that miRNAs, especially miR-126, are involved in many pathologies and that their expression levels increase in autoimmune diseases because they interfere with the transcription of the proteins involved. Since microRNAs can be detected from several biological sources, they may be attractive as potential biomarkers for the diagnosis, prognosis, disease activity and severity of various diseases. In fact, once confirmed the involvement of miR-126 in autoimmune diseases, it was speculated that it could be used as a promising biomarker. These discovers implicate that miR-126 have a central role in many pathways leading to the development and sustain of autoimmune diseases. Its key role make this microRNA a potential therapeutic target in autoimmunity.
Although miR-126 relevant role in several immune-related diseases, further studies are needed to clear its molecular mechanisms; the final step of these novel researches could be the blockage or the prevention of the diseases onset by creating of new targeted therapy.
Micro-RNA represent a great family of small non-condign ribonucleic acid molecules (RNA) ; in particular microRNA-126 (miRNA-126, miR-126) is an important member of this family, encoded by 7th intron of the EGFL7 gene in human chromosome 9q34.3 and expressed in many humans cells such as cardiomyocytes, endothelial and lung cells .
miR-126 aroused many interest, especially in the epigenetic studies, because of its ability to bind directly the DNA, preventing the transcription, translation and degradation of mRNA . As described above, miR-126 and EGFL7 are intimately correlated ; EGFL7 results to be involved in the balance of blood vessels, cell migration and maturation/formation of T-helper 2 cells. These conditions make EGFL7 and miR-126 targets of relevant importance for many diseases such as tumours and autoimmune diseases .
Some studies shown the implication of miR-126 in cancer; recently, significant progress have also been made in determining the role of miR-126 in the regulation of the immune-related diseases [5–7]. As reported by some researchers, microRNAs are involved in the immune response and are associated to autoimmune diseases (i.e. Lupus, Rheumatoid Arthritis) ; probably, in a near future, they could potentially serve as diagnostic biomarkers or therapeutic targets .
The purpose of this review is to investigate the role of miR-126 in autoimmune diseases so as to offer innovative therapies.
Based on the data obtained from literature results, it was concluded that microRNAs are involved in many disorders [57–60]. Their expression levels increase in autoimmune diseases because they interfere with the transcription of the proteins involved .
According data collected, since microRNAs can be detected from several biological sources, they may be attractive as potential biomarkers for the diagnosis, prognosis, disease activity and severity in several diseases . In fact, once confirmed the involvement of miR-126 in autoimmune diseases, it was clear that it could also be used as a promising biomarker.
Previous studies also showed how miR-126 expression could be influenced by modern therapies. Meira et al. analyzed MS patients and confirmed the up-regulation of miR-126 in the immune disease. In addition, they showed that natalizumab (a inhibitory molecule that binds α4β1- and α4β7 integrins) could influence miR-126 expression, normalising it . In particular, Meira and colleagues evaluated the expression of miR-126 in CD4+ T cells obtained from the serum of natalizumab-treated patients noticing a significant down-regulation of the miRNA . Another group demonstrated the important role of Sifalimumab (a human anti–IFN monoclonal antibody which specifically neutralizes most IFN subtypes, preventing signaling through the type I IFN receptor) in SLE. They showed that Sifalimumab decreased miR-126 expression in SLE .
These discovers implicate that miR-126 have a central role in many pathways leading to the development and the sustain of autoimmune diseases. Its key role could let us speculate this microRNA to be a potential therapeutic target in autoimmunity. All the papers reviewed emphasize its relationship with the innate and the adaptive immune response. More pathophysiological studies should consider it as the fulcrum for possible therapeutic approaches. Although miR-126 relevant role, further researches could be useful to find many of its molecular mechanisms in order to block or prevent the onset of the diseases by considering targeted therapy; biological drugs/monoclonal therapies together with the transfection with miRNA plasmids or the usage of inhibitors could represent a path to follow. Decreasing the side effects while obtaining more effective treatments for patients could be an achievable objective.
CR and SG designed the study, made studies analysis and interpretation, and revised the manuscript. MC, EDS and TB carried out the bibliographic search, contributed to the draft of the manuscript. MC and EDS wrote and coordinated the draft of the manuscript. All authors read and approved the final manuscript.
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The authors declare that they have no competing interests.
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