Role of long noncoding RNA-MALAT1 in human peritoneal mesothelial cells fibrosis induced with high glucose

Abstract

Objective To study the role of long noncoding RNA-MALAT1 in human peritoneal mesothelial cells (HPMCs) fibrosis induced with high glucose (HG). Methods The expression of MALAT1, E-cadherin, alpha-smooth muscle actin (ɑ-SMA), collagenⅠ, collagen Ⅲ, fibronectin, and connective tissue growth factor (CTGF) were tested by real-time PCR and Western blot in HPMCs incubated with HG medium (50 mmol/L glucose) or in control medium for different time (for 0, 1, 3, 5, and 7 days). The expression of MALAT1, E-cadherin, ɑ-SMA, collagenⅠ, collagenⅢ, fibronectin, and CTGF were also assayed by real-time PCR and Western blot in HPMCs after transfection with MALAT1 lentivirus, or control lentivirus. MALAT1 small interfering RNA (siRNA), or control siRNA was transfected into HPMCs that had been cultured with HG medium for 72 hours. Results The expression of MALAT1, ɑ-SMA, collagenⅠ, collagenⅢ, fibronectin, and CTGF in HPMCs cultured with HG medium for 72 hours were significantly increased (P<0.05), but E-cadherin decreased with the stimulation time of HG (P<0.05). Compared with control lentivirus, the expression of MALAT1, ɑ-SMA, collagenⅠ, collagenⅢ, fibronectin, and CTGF were increased, but E-cadherin was reduced after transfection with the MALAT1 lentivirus (P<0.01), suggesting that overexpression of MALAT1 might lead to an increase in epithelial-mesenchymal transition (EMT) and fibrosis of HPMCs. The expression of MALAT1, ɑ-SMA, collagen, collagenⅢ, fibronectin, and CTGF decreased (P<0.05), but E-cadherin increased (P<0.05) after silencing the expression of MALAT1 by siRNA compared with the control cells, demonstrating that down-regulation of MALAT1 could inhibit EMT and fibrosis in HG-induced HPMCs. Conclusion MALAT1 might participate in and promote the HG-induced fibrosis and damage of HPMCs. Key words: Peritoneal fibrosis; Epithelial-mesenchymal transition; LncRNA; MALAT1