TNFα up-regulates COX-2 in chronic progressive nephropathy through nuclear accumulation of RelB and NF-κB2. (14th March 2016)

• Record Type: Journal Article
• Authors: Qiu, Junsi; Yuan, Hongying; Chen, Shujue; Zhou, Ying; Song, Dan; Chen, Rongquan
• Is Part Of: Archives of physiology and biochemistry. Volume 122:Number 2(2016)
• Page Start: 88
• Page End: 93
• Publication Date: 2016-03-14
• Subjects: TNFα -- cyclooxygenase-2 -- TNFα-RelB/p52 pathway -- renal damage -- anti-thymocyte serum nephropathy -- inflammatory; Physiology -- Periodicals; Biochemistry -- Periodicals; Biophysics -- Periodicals; Biochemistry; Physiology; 571
• DOI: 10.3109/13813455.2016.1141961
• Languages: English
• ISSNs: 1381-3455

Abstract

Abstract: Objective : The pathogenesis of progressive nephropathies involves inflammatory factors. The inhibition of cyclooxygenase-2 (COX-2) can limit renal damage and inflammation. However, the mechanism of up-regulation of COX-2 in nephropathy is poorly defined. Materials and methods : Here we found that tumor necrosis factor alpha (TNFα) was involved in expression of COX-2 in normal rat kidney (NRK) cell line. Results : TNFα stimulated COX-2 production in a time-dependent manner in NRK cells by inducing nuclear accumulation of RelB and nuclear factor kappa B2 (NF-κB2) and their association with COX-2 gene promoter. Depletion of IκB-inducing kinase alpha, a positive regulator of activation of p100 processing to active p52, attenuated TNFα-induced COX-2 production. Furthermore, TNFα induced COX-2 production and nuclear import in anti-thymocyte serum (ATS) nephropathy. Discussion and conclusion : These data suggest that TNFα-RelB/p52 pathway may be involved in the early stages of renal damage, in part by stimulating COX-2 and inflammatory responses.