LncRNA PTTG3P induced aberrant glycosylated IgA1 production and B cell growth in IgA nephropathy.

Growing evidences suggested that lncRNAs played functional role in several cell functions such as cell growth, invasion, migration, metabolize, apoptosis, and differentiation. However, roles of lncRNA in the development and progression of IgAN remain unknown. In this reference, we indicated that PTTG3P level was overexpressed in IgAN samples compared to healthy subject. PTTG3P expression was also higher in urinary of IgAN cases than in urinary of healthy control. Furthermore, the urinary expression of PTTG3P was correlated with PTTG3P expression in intra-renal of IgAN cases. PTTG3P overexpression induced B cell growth and enhanced cyclin D1 and ki-67 expression. Overexpression of PTTG3P induced IL-1β and IL-8 production. miR-383 level was decreased in IgAN samples compared to healthy subject. In addition, miR-383 expression was also lower in urinary of IgAN cases than in urinary of healthy control. Elevated miR-383 expression decreased luciferase intensity regulated with PTTG3P, while overexpression of miR-383 had no effect on luciferase intensity of the mutant PTTG3P. PTTG3P overexpression suppressed miR-383 expression in B cells. Ectopic miR-383 expression suppressed B cell growth and IL-1β and IL-8 production. Finally, we showed that overexpression of PTTG3P promoted B cell growth and IL-1β and IL-8 production via regulating miR-383. There results proved that PTTG3P played crucial role in progression of IgAN.