Circ_0000524/miR‐500a‐5p/CXCL16 axis promotes podocyte apoptosis in membranous nephropathy

Abstract

Background Podocytes apoptosis is a hallmark of membranous nephropathy (MN). Circ_0000524 has been reported to be associated with patients with MN, whereas the effect of circ_0000524 on podocytes apoptosis and the underlying mechanisms in MN have not been elaborated. Methods Quantitative real‐time polymerase chain reaction (qRT‐PCR) and Western blot were performed to detect the expressions of circ_0000524, microRNA‐500a‐5p (miR‐500a‐5p), and C‐X‐C chemokine ligand 16 (CXCL16) in MN tissues and podocytes. Podocyte injury was induced by angiotensin II (AngII). Cell apoptosis was detected by flow cytometry. Caspase‐3 or caspase‐9 activity was evaluated using a caspase‐3 or caspase‐9 activity assay kit, respectively. Dual‐luciferase reporter assay, RNA immunoprecipitation (RIP) and pull‐down assay were used to address the relationship among circ_0000524,miR‐500a‐5p and CXCL16. Results Upregulation of circ_0000524 and CXCL16 and low expression of miR‐500a‐5p were observed in MN tissues. AngII treatment induced the overexpression of circ_0000524 and CXCL16, a decrease of miR‐500a‐5p, and induced cell apoptosis in podocytes. Circ_0000524 negatively modulated the expression of miR‐500a‐5p. Circ_0000524 depletion inhibited podocyte apoptosis, which was rescued by loss of miR‐500a‐5p. miR‐500a‐5p contained the binding sites with CXCL16. Circ_0000524 knockdown hampered CXCL16 expression by upregulating miR‐500a‐5p expression. Additionally, miR‐500a‐5p upregulation suppressed AngII‐induced podocyte apoptosis, which was rescued by enhanced expression of CXCL16. Conclusion Circ_0000524/miR‐500a‐5p/CXCL16 pathway regulated podocyte apoptosis in MN.

circRNA_0001679/miR-338-3p/DUSP16 axis aggravates acute lung injury

“…However, the biological function of circ_0001679 in sepsis-induced ALI progression remains unclear. Moreover, circRNAs can act as microRNA (miRNA) “sponges” and upregulate the target gene by isolating and competitively inhibiting miRNA activity [ 17 ], thereby modulating progression of diseases [ 18 , 19 , 20 ]. We intended to explore whether circ_0001679 exerts its function in sepsis-induced ALI in such manner.…”

Serum Protein Signatures Using Aptamer-Based Proteomics for Minimal Change Disease and Membranous Nephropathy

“…30 Increased apoptosis in MN was another hallmark observed in our protein signature data and is consistent with glomerular injury that results in cell death and loss of podocytes. 31,32 In contrast, MCD generally displayed a different immune profile and reduced cell death but enhanced vascular functions compared with MN. For example, several proteins involved in adaptive immunity were dysregulated in MCD, including CD40LG, CSF1, TNFRSF17, CCL21, and STAT1/3, in keeping with the proposed disease pathogenesis that involves T and B lymphocytes.…”

CircRNAs as Potential Blood Biomarkers and Key Elements in Regulatory Networks in Gastric Cancer

“…We found its expression was significantly upregulated in blood GC samples, but not in tissue. The only reports of circRBM23 in the literature are of its upregulation in both a kidney disease called membranous nephropathy [ 40 ] and in HCC [ 41 ]. In HCC, circRBM23 was able to modulate cell viability and migration in vitro, and tumorigenesis in vivo, through the miR-138/vimentin- CCND3 axis [ 41 ].…”