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TNFα up-regulates COX-2 in chronic progressive nephropathy through nuclear accumulation of RelB and NF-κB2

Junsi Qiu1, Hongying Yuan1, Shujue Chen1

  • 1a Department of Nephrology , Nanjing Medical University Affiliated Wuxi Second Hospital , Wuxi , Jiangsu , China.

Archives of Physiology and Biochemistry
|January 30, 2016
PubMed
Abstract

Insights

Tumor necrosis factor alpha (TNFα) upregulates cyclooxygenase-2 (COX-2) in kidney cells. This TNFα-RelB/p52 pathway may drive early renal damage and inflammation in progressive nephropathies.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Inflammation Research

Background:

  • Progressive nephropathies are driven by inflammation.
  • Cyclooxygenase-2 (COX-2) inhibition can mitigate renal damage.
  • The precise mechanisms of COX-2 upregulation in nephropathy remain unclear.

Purpose of the Study:

  • To elucidate the role of tumor necrosis factor alpha (TNFα) in COX-2 expression within kidney cells.
  • To investigate the signaling pathway responsible for TNFα-induced COX-2 upregulation.
  • To determine if this pathway is active in anti-thymocyte serum (ATS) nephropathy.

Main Methods:

  • Utilized normal rat kidney (NRK) cell lines.
  • Investigated TNFα's effect on COX-2 production and nuclear factor localization.
  • Examined the impact of depleting IκB-inducing kinase alpha.
  • Assessed TNFα and COX-2 expression in a rat model of ATS nephropathy.

Main Results:

  • TNFα stimulation led to time-dependent COX-2 production in NRK cells.
  • TNFα induced nuclear accumulation of RelB and nuclear factor kappa B2 (NF-κB2), associating with the COX-2 promoter.
  • Depletion of IκB-inducing kinase alpha reduced TNFα-induced COX-2 production.
  • TNFα promoted COX-2 production and nuclear import in the context of ATS nephropathy.

Conclusions:

  • The TNFα-RelB/p52 signaling pathway is implicated in COX-2 upregulation.
  • This pathway may contribute to early renal damage by enhancing inflammatory responses.
  • Targeting the TNFα-RelB/p52 pathway could offer therapeutic strategies for nephropathies.
Keywords:
TNFαTNFα-RelB/p52 pathwayanti-thymocyte serum nephropathycyclooxygenase-2inflammatoryrenal damage

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