Basic & Clinical Medicine ›› 2018, Vol. 38 ›› Issue (10): 1389-1396.

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RIPK2-mediated autophagy on the activation of ROS, caspase-1 and IL-1β in high glucose-induced mouse glomerular mesangial cells


  • Received:2017-09-28 Revised:2017-12-03 Online:2018-10-05 Published:2018-09-28

Abstract: Objective To investigate the effect of receptor interacting serine/threonine protein kinase 2(RIPK2) mediated autophagy on the activation of ROS, caspase-1 and IL-1β in high glucose-induced glomerular mesangial cells(GMCs). Methods GMCs were exposed to highglucose,RIPK2 was suppressed by NLRP3-specifc siRNA; autophagy was observed by mRFP-GFP-LC3fusion protein with confocal microscope; intracellular ROS level was detected by DCFH-DA fluorescent probe; the protein and mRNA expression of RIPK2,LC3II/I, caspase-1 and IL-1βweredetectedby Western blot and RT-PCR; the release of IL-1β was detected by ELISA. Results 1)The intracellular ROS and the expression of caspase-1 and IL-1β were increased by high glucose in a time and dose-dependent manner (P<0.05).2)The expression of RIPK2 and LC3II/I were increased by high glucosefor0-12h(P<0.05), but these proteins weredown-regulated following high glucose over 12 h(P<0.05). 3)LC3II/I expression were decreased but intracellular ROS, caspase-1 and IL-1β expression were significantly facilitated by siRNA-RIPK2(P<0.05). Conclusions RIPK2-mediated autophagy negatively regulates the activation of ROS, caspase-1 and IL-1β induced by high glucose, suggesting that a potential target for prevention and control of diabetic kidney disease(DKD).

Key words: RIPK2, autophagy, ROS, diabetic kidney disease