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Background   Sumoylation is extensively involved in the regulation of NF- κ B signaling. PIASy, as a SUMO E3 ligase, has been proved to mediate sumoylation of I κ B kinase  γ  (IKK γ ) and contribute to the activation of NF- κ B under genotoxic agent stimulation. However, the association of PIASy and NF- κ B signaling in the pathogenesis of diabetic nephropathy (DN) has not been defined.Methods   Rat glomerular mesangial cells (GMCs) were stimulated by high glucose; siRNA was constructed to silence the expression of PIASy; the expression of PIASy, SUMO isoforms (SUMO1, SUMO2/3), and NF- κ B signaling components was analyzed by Western blot; the interaction between IKK γ  and SUMO proteins was detected by coimmunoprecipitation; and the release of inflammatory cytokines MCP-1 and IL-6 was assayed by ELISA.Results   High glucose significantly upregulated the expression of PIASy, SUMO1, and SUMO2/3 in a dose- and time-dependent manner ( P  < 0.05), induced the phosphorylation and sumoylation of IKK γ  ( P  < 0.05), and then triggered NF- κ B signaling whereas MCP-1 and IL-6 were released from GMCs ( P  < 0.05). Moreover, these high glucose-induced effects were observably reversed by siRNA-mediated knockdown of PIASy ( P  < 0.05).Conclusion   The SUMO E3 ligase PIASy mediates high glucose-induced activation of NF- κ B inflammatory signaling, suggesting that PIASy may be a potential therapeutic target of DN.

SUMO E3 Ligase PIASy Mediates High Glucose-Induced Activation of NF-κB Inflammatory Signaling in Rat Mesangial Cells