Abstract
Ankylosing spondylitis (AS) is a chronic systemic autoimmune disease characterized by inflammation, bone erosion, spur formation of the spine and the sacroiliac joints. However, the etiology and molecular pathogenesis of AS remain largely unclear. Recently, a growing number of studies showed that long non-coding RNAs (lncRNAs) played critical roles in the development and progression of autoimmune and orthopedic conditions, including AS. Studies demonstrated that a myriad of lncRNAs (e.g. H19, MEG3, LOC645166) pertinent to regulation of inflammatory signals were deregulated in AS. A number of lncRNAs might also serve as new biomarkers for the diagnosis and predicting the outcomes of AS. In this review, we summarize lncRNA profiling studies on AS and the functional roles and mechanism of key lncRNAs relevant to AS pathogenesis. We also discuss their potential values as biomarkers and druggable targets for this potentially disabling condition.
Highlights
Ankylosing spondylitis (AS) is a chronic systemic autoimmune-mediated inflammatory disease, which primarily affects the spine and the sacroiliac joints and causes pain and stiffness of these joints [1,2,3,4,5]
We summarize the deregulation of another important class of non-coding RNA, namely long non-coding RNAs (lncRNAs), in AS in relation to their biological functions and molecular mechanisms, sponging of miRNAs
In AS, differentially expressed lncRNAs have been identified at transcriptome-wide level by RNA sequencing or microarray in hip joint ligament, peripheral blood, peripheral blood mononuclear cells (PBMCs), or osteogenically differentiated mesenchymal stem cells (MSCs)
Summary
Ankylosing spondylitis (AS) is a chronic systemic autoimmune-mediated inflammatory disease, which primarily affects the spine and the sacroiliac joints and causes pain and stiffness of these joints [1,2,3,4,5]. HLA-B27 accounts for 20% of the total AS heritability It encodes a major histocompatibility complex (MHC) Class I protein that is prone to misfolding in the endoplasmic reticulum (ER) and abnormal dimerization on cell surface as compared to proteins encoded by other HLA loci. Emerging evidence support that dysregulation of non-coding RNAs, including miRNAs and lncRNAs, is pivotal to AS pathogenesis In this connection, we previously reviewed the roles of miRNAs in AS, highlighting their involvements in modulating immune cell functions, such as cytokine response and T-cell survival [52]. We summarize the deregulation of another important class of non-coding RNA, namely lncRNAs, in AS in relation to their biological functions and molecular mechanisms, sponging of miRNAs. We discuss the potential utilization of serum and tissue lncRNAs as diagnostic or prognostic markers as well as druggable targets for AS
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