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Interleukin-7 stimulation inhibits nephrin activation and induces podocyte injury

Shubo Zhai1, Lengyue Zhao1, Yan Zhang1

  • 1Department of Pediatric Nephropathy, The First Hospital of Jilin University, China.

Biochemical and Biophysical Research Communications
|November 21, 2018
PubMed

Insights

Interleukin-7 receptor (IL-7R) is induced in kidney podocytes during nephrotic syndrome. IL-7R activation causes podocyte injury and impairs kidney filtration, suggesting IL-7R as a therapeutic target for nephrotic syndrome.

Area of Science:

  • Nephrology
  • Immunology
  • Cell Biology

Background:

  • Glomerular podocytes are crucial for kidney filtration barrier integrity.
  • Disturbances in podocyte function are implicated in idiopathic nephrotic syndrome (INS), a pediatric kidney disease.

Purpose of the Study:

  • To investigate the role of interleukin-7 receptor (IL-7R) in adriamycin (ADR)-induced mouse nephropathy, a model for nephrotic syndrome.
  • To determine the functional impact of IL-7R activation on podocyte injury and kidney filtration.

Main Methods:

  • Adriamycin (ADR) administration to induce nephropathy in mice.
  • In vitro culture of mouse podocytes exposed to ADR.
  • Stimulation of IL-7R with recombinant IL-7.
  • Assessment of podocyte apoptosis, nephrin activation, and actin cytoskeleton organization.
  • Evaluation of podocyte monolayer filtration barrier function.

Main Results:

  • IL-7 receptor (IL-7R) expression was upregulated in glomeruli of ADR-induced nephropathy mice and in ADR-treated mouse podocytes.
  • IL-7 stimulation induced podocyte apoptosis, inhibited nephrin activation, and disorganized the actin cytoskeleton.
  • IL-7 stimulation impaired the filtration barrier function of podocyte monolayers.

Conclusions:

  • Interleukin-7 (IL-7) and its receptor (IL-7R) are identified as potential regulators of podocyte function.
  • IL-7R signaling contributes to podocyte injury and filtration barrier dysfunction.
  • IL-7 and IL-7R represent a potential novel therapeutic target for treating idiopathic nephrotic syndrome (INS).

Keywords:
Idiopathic nephrotic syndromeInterleukin-7Nephrin activationPodocyte

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