It is estimated that miRNAs account for 1�C5% of expressed genes in the animal genome and about 20�C30% of all human mRNA are known to be miRNA targets. Because miRNA function as managers in gene regulatory networks, they are distinct from other biomarkers because they may have an upstream and potentially pathogenic role in the disease process. Quantitation of miRNA gene expression levels has become an essential step in understanding mechanisms for cellular processes such as cell differentiation, cell proliferation and cell death, and has shown great promise in identifying effective biomarkers that correlate with human diseases. Although dysregulation of miRNA expression has been characterized mostly in Clobetasol propionate cancer, it has recently been studied in many other diseases. Specifically, miRNA have been proposed as a regulator of immune cell development, playing a role in the inflammatory response and as a key player in the pathogenesis of neurodegenerative diseases. The relationship between SLE and miRNA was first reported by Dai et al who studied the relationship in PBMCs and renal biopsies obtained from Chinese SLE patients. The role miRNA play in autoimmune diseases is incomplete or only beginning to be characterized especially with regard to miRNA. However, the importance of miRNA on post-transcriptional regulation of gene expression in SLE is emerging with some surprising results. In one relevant example a mouse model of SLE with defects in miRNA regulation of mRNA FK-3311 induced disease. Here miRNA101 suppresses expression of the ICOS, which is defective in sanroque model of lupus, leading to stimulation of autoreactive B cells and a lupus-like illness. Understanding the role of miRNA in SLE may have important implications for disease pathology. We evaluated miRNA expression by microarray technology in samples obtained from lupus nephritis patients and unaffected controls. In these samples we identified changes in miRNA expression that correlate with lupus. Five miRNA were differentially expressed across different racial groups and in all specimen types tested.
Because miRNA function as managers in gene regulatory networks
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