MiR-320 promotes B cell proliferation and the production of aberrant glycosylated IgA1 in IgA nephropathy

J Cell Biochem. 2018 Jun;119(6):4607-4614. doi: 10.1002/jcb.26628. Epub 2018 Feb 27.

Abstract

IgA nephropathy (IgAN) is one of the most common primary glomerulonephritis. However, the etiology of this disease is complex and the pathogenesis of IgAN is still unknown. MicroRNAs (miRNAs) play important roles in a lot of pathological and physiological processes. In this study, we showed that the expression of miR-320 was significantly upregulated in renal tissues and urinary of IgAN patients. Moreover, the intra-renal expression level of miR-320 had significant correlation with miR-320 expression in the urinary of IgAN patients. Overexpression of miR-320 increased B cell proliferation and promoted cyclin D1 expression. Furthermore, we identified that PTEN was direct target gene of miR-320 in the B cell. Ectopic expression of miR-320 suppressed PTEN expression. Overexpression of miR-320 decreased Cosmc expression in the B cell. In addition, we demonstrated that Cosmc expression was significantly downregulated in the renal tissues and urinary of IgAN patients. The intra-renal expression level of Cosmc had significant correlation with Cosmc expression of urinary in IgAN patients. We proved that the expression level of Cosmc was negatively correlated with the expression of miR-320 in the renal tissues of IgAN patients. Overexpression of miR-320 promoted the B cell proliferation through suppressing PTEN expression. Taken together, these data suggested that miR-320 acted an important role in the development of IgAN.

Keywords: B cell; IgA nephropathy; IgAN; miR-320; microRNAs.

MeSH terms

  • B-Lymphocytes / metabolism*
  • B-Lymphocytes / pathology
  • Cell Line
  • Cell Proliferation*
  • Cyclin D1 / biosynthesis
  • Gene Expression Regulation
  • Glomerulonephritis, IGA / metabolism*
  • Glomerulonephritis, IGA / pathology
  • Humans
  • Immunoglobulin A / biosynthesis*
  • Kidney / metabolism*
  • Kidney / pathology
  • MicroRNAs / metabolism*
  • Molecular Chaperones / biosynthesis
  • PTEN Phosphohydrolase / biosynthesis

Substances

  • C1GALT1C1 protein, human
  • CCND1 protein, human
  • Immunoglobulin A
  • MIRN320 microRNA, human
  • MicroRNAs
  • Molecular Chaperones
  • Cyclin D1
  • PTEN Phosphohydrolase
  • PTEN protein, human