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Aim: We aimed to explore the detailed molecular mechanism of immune‐associated genes in membranous nephropathy (MN). Methods: A microarray data set (GSE133288) was retrieved from the Gene Expression Omnibus database. Differentially expressed mRNAs (DEMs) in MN vs control groups were identified, and MN‐related DEMs (MN‐DEMs) were further verified and screened using the comparative toxicogenomics database (CTD) database. The publicly available database, InnateDB was used to investigate immune genes, and the overlapped genes between MN‐DEMs and the immune genes were considered as MN‐related immune genes (iDEMs). A protein‐protein interaction network (PPI) was constructed based on these iDEMs, followed by function and pathway enrichment analysis. Finally, microRNAs (miRNAs) and long noncoding RNAs (lncRNAs) associated with iDEMs were predicted, followed by a lncRNA‐miRNA‐mRNA (competing endogenous RNAs, ceRNA) network construction. Results: A total of 327 DEMs and 48 iDEMs were revealed; a PPI network was constructed with 100 PPI pairs and 37 iDEMs. iDEMs including JUN and FOS were mainly enriched in pathways such as osteoclast differentiation and function including response to immobilization stress, respectively. Based on mRNA‐associated miRNA and lncRNA prediction, 30 ceRNA interactions including KCNQ1OT1‐miR‐204‐5p‐SRY‐Box Transcription Factor 4 (SOX4) were explored. Conclusion: mRNAs including FOS and JUN might participate in MN development via response to immobilization stress function and the osteoclast differentiation pathway. The mRNA SOX4 might contribute to MN progression via sponging KCNQ1OT1‐miR‐204‐5p interaction. SUMMARY AT A GLANCE: The authors investigated differentially expressed mRNA's in membranous nephropathy (MN) vs controls from a microarray data set, and identified that mRNAs including FOS and JUN might participate in MN development with SOX4 potentially contributing to MN progression. These findings assist with better understanding the molecular processes underpinning MN especially pertaining to the involvement of immune‐associated gene expression. [ABSTRACT FROM AUTHOR]

Podocytes are an important component of the glomerular filtration barrier in the kidneys. The dysfunction and apoptosis of podocytes are important factors that can lead to the progression of chronic kidney disease (CKD). In CKD, angiotensin II is continuously elevated in circulation and is considered to have key roles in inducing podocyte injury and apoptosis. Curcumin is a hydrophobic polyphenolic compound extracted from turmeric. Increasing evidence demonstrates that curcumin has a protective effect on the kidneys in CKD. However, the mechanisms mediating this protective effect remain unclear. The aim of this study was to explore whether curcumin could protect against angiotensin II‐induced injury and apoptosis of podocytes. We performed western blotting, immunofluorescence, phalloidin staining, and terminal deoxynucleotidyl transferase nick‐end labeling staining to observe the expression level of podocyte‐specific proteins, apoptosis‐related proteins, and the arrangement of F‐actin. We found that curcumin could reverse angiotensin II‐induced podocyte injury and apoptosis in a dose‐dependent manner. In addition, curcumin dose‐dependently attenuated a pro‐apoptotic pathway, activated by angiotensin II‐induced endoplasmic reticulum stress. Conversely, the protective effects of curcumin were impaired upon addition of tunicamycin, an activator of endoplasmic reticulum stress. Thus, we speculate that curcumin protects against angiotensin II‐induced podocyte injury and apoptosis, at least partly by inhibiting endoplasmic reticulum stress. [ABSTRACT FROM AUTHOR]