Abstract
Increasing evidence shows miR-155 plays an important role in regulating inflammatory processes in systemic lupus erythematosus (SLE), especially in lupus nephritis (LN). Because the chemokine CXCL13 is implicated in the pathogenesis of LN, here we examined whether miR-155 can modulate the activity of CXCL13 or its receptor CXCR5. We determined the expression of CXCL13 in normal and MRL/lpr mice and found elevated levels of CXCL13 in the kidneys of MRL/lpr mice compared with normal kidneys. Besides, CXCL13 expression was mainly detected in the glomerulus, specifically to mesangial areas. We then transfected a miR-155 mimic in human renal mesangial cells (HRMCs) to overexpress miR-155 and detected decreased protein levels of CXCR5 by western blot analysis. Transfection of the miR-155 mimic into CXCL13-treated HRMCs resulted in a significantly reduced proliferation rate of HRMCs as measured by the cell-counting assay and flow cytometry. Moreover, increased intracellular miR-155 also led to decreased phosphorylation of ERK and TGF-β1 production. Together, these results revealed that miR-155 may play a role in the pathogenesis of LN.
Highlights
Systemic lupus erythematosus (SLE) is an autoimmune disease with immune complexes formation and deposition in multiple organs, among which, the kidney is one of the major target organs [12, 34]
We found that the expression levels of CXCL13 in the kidneys of MRL/lpr mice were significantly increased in comparison to normal mice (Fig. 1 and Fig. 2)
Increasing evidence indicates that many miRNAs such as miR-146, miR-21, and miR-155 have the ability to negatively regulate the activation of inflammatory pathways in myeloid cells, suggesting they have anti-inflammatory effects [20]
Summary
Systemic lupus erythematosus (SLE) is an autoimmune disease with immune complexes formation and deposition in multiple organs, among which, the kidney is one of the major target organs [12, 34]. 1 Department of Rheumatology, Affiliated Hospital of Nantong University, SLE patients have lupus nephritis (LN), and almost all patients have pathological kidney involvement [2, 6]. 10% of LN patients progress to end-stage renal disease (ESRD) [16]. The mortality rate within 1–5 years in severe refractory LN patients is still high [1]. It is of great importance to explore the pathogenesis of LN and search for new therapeutic targets
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
