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Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Transl+Med 2015 ; 13 (ä): ä Nephropedia Template TP
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Anti-dsDNA antibodies induce inflammation via endoplasmic reticulum stress in human mesangial cells #MMPMID26040555
Zhang H; Zhao C; Wang S; Huang Y; Wang H; Zhao J; Yang N
J Transl Med 2015[]; 13 (ä): ä PMID26040555show ga
Background: Anti-dsDNA antibodies play an important role in the pathogenesis of lupus nephritis (LN). Endoplasmic reticulum (ER) stress is a physical reaction under stressful condition and can cause inflammation when stimulation is sustained. This study investigated the roles of ER stress in anti-dsDNA antibody-induced inflammation response in human mesangial cells (HMCs). Method: Anti-dsDNA antibodies isolated from LN patients were used to stimulate HMCs. The expression of GRP78, PERK, p-PERK, p-eIF2?, ATF4, p-IRE1?, ATF6 and CHOP in HMCs was measured by western blot. NF-?B activation was detected by examining nuclear translocation of NF-?B p65. The expression and production of IL-1?, TNF-? and MCP-1 were examined by qPCR and ELISA. Results: Flow cytometry and cellular ELISA showed that anti-dsDNA antibodies can bind to HMCs. The binding was not inhibited by blockage of Fc receptor. Anti-dsDNA antibody stimulation significantly enhanced the expression of GRP78, p-PERK, p-eIF2? and ATF4 in HMCs. However, no significant increase in the expression of p-IRE1? and ATF6 was found. In addition, anti-dsDNA antibodies also significantly increased the activation of NF-?B and upregulated the expression of IL-1?, TNF-? and MCP-1, which were suppressed by pretreatment of HMCs with chemical ER stress inhibitor 4-PBA. Transfection of specific ATF4 siRNA also significantly reduced the activation of NF-?B and expression of proinflammatory cytokines. Conclusion: Anti-dsDNA antibodies induce NF-?B activation and inflammation in HMCs via PERK-eIF2?-ATF4 ER stress pathway.