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WNT1-inducible signaling pathway protein 1 regulates kidney inflammation through the NF-κB pathway

Bo Wang1,2, Chenguang Ding1,3, Xiaoming Ding1,3

  • 1Department of Kidney Transplantation, Nephropathy Hospital, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi 710061, P.R. China.

Clinical Science (London, England : 1979)
|December 13, 2021
PubMed

Insights

WNT1-inducible signaling pathway protein 1 (WISP1) drives kidney inflammation by activating nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB). Blocking WISP1 shows potential for treating kidney disease by reducing inflammation.

Area of Science:

  • Nephrology
  • Immunology
  • Molecular Biology

Background:

  • Kidney inflammation is a key factor in kidney injury progression and fibrosis.
  • The role of WNT1-inducible signaling pathway protein 1 (WISP1) in kidney inflammation requires further investigation.

Purpose of the Study:

  • To investigate the regulatory function of WISP1 in kidney inflammation.
  • To explore the potential of targeting WISP1 as a therapeutic strategy for kidney disease.

Main Methods:

  • Administration of recombinant WISP1 protein and WISP1 inhibition (gene knockdown, neutralizing antibody) in mouse models.
  • Assessment of inflammatory markers (macrophage accrual, TNF-α, CCL2, IL-6) and NF-κB signaling.
  • Evaluation in unilateral ureter obstruction (UUO) and streptozotocin (STZ)-induced diabetic nephropathy (DN) models.

Main Results:

  • Recombinant WISP1 induced kidney inflammation, mediated by NF-κB signaling.
  • WISP1 inhibition reduced inflammatory cytokine production in macrophages and fibroblast proliferation.
  • WISP1 expression was elevated in UUO and STZ-induced DN mouse models.
  • WISP1 antibody treatment decreased kidney inflammation in UUO mice.

Conclusions:

  • WISP1 promotes kidney inflammation through NF-κB signaling.
  • Pharmacological blockade of WISP1 presents a potential novel therapeutic approach for kidney inflammation in kidney diseases.
Keywords:
fibroblastsinflammationrenal fibrosisrenal physiology

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