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Bone marrow mesenchymal stem cell-derived exosomes protect podocytes from HBx-induced ferroptosis

Xiaoqian Yang1, Yani Yu1, Baoshuang Li1

  • 1Department of Nephrology, The Affiliated Hospital of Qingdao University, Qingdao, China.

Peerj
|May 16, 2023
PubMed

Insights

Bone marrow mesenchymal stem cell-derived exosomes (BMSC-exosomes) show potential in treating Hepatitis B virus-associated glomerulonephritis (HBV-GN). These exosomes inhibit ferroptosis in kidney podocytes by transferring miR-223-3p, offering a novel therapeutic strategy for HBV-GN.

Area of Science:

  • Nephrology
  • Cell Biology
  • Molecular Medicine

Background:

  • Hepatitis B virus-associated glomerulonephritis (HBV-GN) is a significant cause of kidney disease in China, with unclear pathogenesis and limited treatment options.
  • Podocyte injury and ferroptosis are implicated in HBV-GN progression.

Purpose of the Study:

  • To investigate the protective mechanism of exosomes derived from bone marrow mesenchymal stem cells (BMSCs) against HBV-induced podocyte injury.
  • To elucidate the role of miR-223-3p in this protective process.

Main Methods:

  • Human renal podocytes were transfected with HBx protein to mimic HBV infection.
  • Cell viability, iron content, malondialdehyde (MDA), and reactive oxygen species (ROS) levels were assessed.
  • Expression of ferroptosis-related molecules was analyzed using qRT-PCR and Western blot.
  • The effect of BMSC-derived exosomes and miR-223-3p was evaluated using inhibitors.

Main Results:

  • HBx overexpression reduced podocyte viability and induced ferroptosis, evidenced by altered expression of GPX4, SLC7A11, and ACSL4, and increased iron, MDA, and ROS levels.
  • BMSC-derived exosomes protected podocytes from HBx-induced ferroptosis.
  • miR-223-3p was enriched in BMSC-derived exosomes, and its inhibition reversed the protective effects.

Conclusions:

  • BMSC-derived exosomes exert a protective effect against HBx-induced podocyte ferroptosis.
  • This inhibition occurs through the transfer of miR-223-3p, highlighting a novel therapeutic pathway for HBV-GN.
Abstract

Keywords:
Bone marrow mesenchymal stem cellsExosomesFerroptosisHBxmiR-223-3p

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