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Background <p>Mesenchymal stem cells (MSCs) possess immunomodulatory and tissue repair properties, and their therapeutic efficacy has been reported in models of glomerulonephritis. However, the clinical application of bone marrow-derived MSCs (BMSCs) is limited due to the invasive nature of bone marrow harvesting. In this study, we focused on amnion-derived MSCs (AMSCs), which can be obtained non-invasively after delivery, and investigated their therapeutic effects in a rat model of anti-glomerular basement membrane (GBM) nephritis.</p> Methods <p>In a rat model of anti-GBM nephritis, human AMSCs, BMSCs, or vehicle were intravenously administered. Evaluations included renal function, histology, intravital imaging of glomerular neutrophils, and flow cytometric analysis of leukocytes. In addition, we used an anti-CD44 neutralizing antibody in vivo to examine the therapeutic relevance of CD44 blockade, including its impact on neutrophil.</p> Results <p>The renoprotective effects observed in the AMSC-treated group were comparable to or greater than those in the BMSC-treated group. Furthermore, neutrophils exposed to AMSCs exhibited shorter dwell time in the glomeruli, and specifically in renal neutrophils, the expression of the adhesion molecule CD44 was reduced. In addition, administration of an anti-CD44 antibody produced similar renoprotective effects and reductions in neutrophil infiltration, suggesting that modulation of CD44 signaling contributes to the renoprotective effects of AMSCs.</p> Conclusions <p>Collectively, these findings indicate that AMSCs exert renoprotective effects comparable to or greater than those of BMSCs, and may represent a novel therapeutic approach for anti-GBM nephritis by specifically suppressing CD44 expression in neutrophils at sites of inflammation.</p> Graphical Abstract <p></p>

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Amnion-derived mesenchymal stem cells attenuate anti-GBM glomerulonephritis via regulation of neutrophil CD44 expression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月19日

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  • Tomoya Nozaki,
  • Kumiko Fujieda,
  • Kazuhiro Furuhashi,
  • Yuko Shimamura,
  • Munetoshi Karasawa,
  • Eri Koshi-Ito,
  • Yu Watanabe,
  • Chikao Onogi,
  • Keita Hattori,
  • Akihisa Kato,
  • Jun Matsumoto,
  • Tomohiro Kawazoe,
  • Asuka Horinouchi,
  • Akihito Tanaka,
  • Hangsoo Kim,
  • Kayaho Maeda,
  • Makoto Matsuyama,
  • Kenichi Yamahara,
  • Shoichi Maruyama

摘要

Background

Mesenchymal stem cells (MSCs) possess immunomodulatory and tissue repair properties, and their therapeutic efficacy has been reported in models of glomerulonephritis. However, the clinical application of bone marrow-derived MSCs (BMSCs) is limited due to the invasive nature of bone marrow harvesting. In this study, we focused on amnion-derived MSCs (AMSCs), which can be obtained non-invasively after delivery, and investigated their therapeutic effects in a rat model of anti-glomerular basement membrane (GBM) nephritis.

Methods

In a rat model of anti-GBM nephritis, human AMSCs, BMSCs, or vehicle were intravenously administered. Evaluations included renal function, histology, intravital imaging of glomerular neutrophils, and flow cytometric analysis of leukocytes. In addition, we used an anti-CD44 neutralizing antibody in vivo to examine the therapeutic relevance of CD44 blockade, including its impact on neutrophil.

Results

The renoprotective effects observed in the AMSC-treated group were comparable to or greater than those in the BMSC-treated group. Furthermore, neutrophils exposed to AMSCs exhibited shorter dwell time in the glomeruli, and specifically in renal neutrophils, the expression of the adhesion molecule CD44 was reduced. In addition, administration of an anti-CD44 antibody produced similar renoprotective effects and reductions in neutrophil infiltration, suggesting that modulation of CD44 signaling contributes to the renoprotective effects of AMSCs.

Conclusions

Collectively, these findings indicate that AMSCs exert renoprotective effects comparable to or greater than those of BMSCs, and may represent a novel therapeutic approach for anti-GBM nephritis by specifically suppressing CD44 expression in neutrophils at sites of inflammation.

Graphical Abstract