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<p>For cell therapy to treat heart failure, therapeutic cells should possess the abilities to promote vascularization, remodel tissues, and reduce inflammation. Previously we clarified that CD14<sup>+</sup>-derived myeloid angiogenic cells (MACs) possessed an angiogenic ability. In this paper, we induced strong high anti-inflammatory and tissue-remodeling properties in CD14<sup>+</sup> cells by adding both M-CSF and interleukin-4 to the endothelial medium. This culture condition produced a higher number of adherent cells than MACs and exhibited greater angiogenic capability; we named these cells ‘MIL4-MACs’. Through analysis of cytokine production, gene expression, and membrane markers, MIL4-MACs were characterized as anti-inflammatory cells, with lower expression of HLA-Class Ⅱ and higher expression of PD-L1 and PD-L2 compared to MACs. Mixed lymphocyte reaction analysis showed that T cells did not attack MIL4-MACs. Moreover, MIL4-MACs expressed active-matrix metalloproteinase-9 on their surface and had high collagen-degrading activity. Administration of MIL4-MACs improved angiotensin Ⅱ‒induced severe cardiac failure and attenuated cardiac fibrosis in mice. These data indicate that the anti-inflammatory, angiogenic, and remodeling properties of MIL4-MACs may represent a novel candidate for cell therapy in heart failure.</p>

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Anti-inflammatory myeloid angiogenic cells (MIL4-MACs) attenuate angiotensin II‒induced heart failure in mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月6日

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  • Toshie Kanayasu-Toyoda,
  • Takeshi Tanaka,
  • Kenji Yoshihara,
  • Goki Matsumura,
  • Katsuhiko Hayashi,
  • Hanayuki Okura,
  • Akifumi Matsuyama,
  • Eriko Uchida,
  • Teruhide Yamaguchi

摘要

For cell therapy to treat heart failure, therapeutic cells should possess the abilities to promote vascularization, remodel tissues, and reduce inflammation. Previously we clarified that CD14+-derived myeloid angiogenic cells (MACs) possessed an angiogenic ability. In this paper, we induced strong high anti-inflammatory and tissue-remodeling properties in CD14+ cells by adding both M-CSF and interleukin-4 to the endothelial medium. This culture condition produced a higher number of adherent cells than MACs and exhibited greater angiogenic capability; we named these cells ‘MIL4-MACs’. Through analysis of cytokine production, gene expression, and membrane markers, MIL4-MACs were characterized as anti-inflammatory cells, with lower expression of HLA-Class Ⅱ and higher expression of PD-L1 and PD-L2 compared to MACs. Mixed lymphocyte reaction analysis showed that T cells did not attack MIL4-MACs. Moreover, MIL4-MACs expressed active-matrix metalloproteinase-9 on their surface and had high collagen-degrading activity. Administration of MIL4-MACs improved angiotensin Ⅱ‒induced severe cardiac failure and attenuated cardiac fibrosis in mice. These data indicate that the anti-inflammatory, angiogenic, and remodeling properties of MIL4-MACs may represent a novel candidate for cell therapy in heart failure.