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<p>Preterm birth disrupts intestinal epithelial maturation, impairing digestive and absorptive functions. This study integrates analysis of single-cell RNA sequencing datasets, spanning fetal to adult stages, with human preterm intestinal models derived from the ileal tissue of preterm infants. We investigate the potential of extracellular vesicles (EVs) derived from human Wharton’s jelly mesenchymal stem cells to promote intestinal maturation. Distinct enterocyte differentiation trajectories are identified during the transition from immature to mature stages of human intestinal development. EV treatment, particularly with the EV39 line, significantly upregulates maturation-specific gene expression related to enterocyte function. Gene set enrichment analysis reveals an enrichment of TGFβ1 signaling pathways, and proteomic analysis identifies TGFβ1 and FGF2 as key mediators of EV39’s effects. These treatments enhance cell proliferation, epithelial barrier integrity, and fatty acid uptake, primarily through CFTR-dependent mechanisms—unique to human preterm models, not observed in mouse intestinal organoids. This highlights the translational potential of EV39 and CFTR activation in promoting the functional maturation of the premature human intestine.</p><p></p>

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Functional maturation of preterm intestinal epithelium through CFTR activation

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年4月2日

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  • Jihyun Kim,
  • Hyunji Park,
  • Na-Young Park,
  • Se In Hwang,
  • Young Eun Kim,
  • Se In Sung,
  • Yun Sil Chang,
  • Ara Koh

摘要

Preterm birth disrupts intestinal epithelial maturation, impairing digestive and absorptive functions. This study integrates analysis of single-cell RNA sequencing datasets, spanning fetal to adult stages, with human preterm intestinal models derived from the ileal tissue of preterm infants. We investigate the potential of extracellular vesicles (EVs) derived from human Wharton’s jelly mesenchymal stem cells to promote intestinal maturation. Distinct enterocyte differentiation trajectories are identified during the transition from immature to mature stages of human intestinal development. EV treatment, particularly with the EV39 line, significantly upregulates maturation-specific gene expression related to enterocyte function. Gene set enrichment analysis reveals an enrichment of TGFβ1 signaling pathways, and proteomic analysis identifies TGFβ1 and FGF2 as key mediators of EV39’s effects. These treatments enhance cell proliferation, epithelial barrier integrity, and fatty acid uptake, primarily through CFTR-dependent mechanisms—unique to human preterm models, not observed in mouse intestinal organoids. This highlights the translational potential of EV39 and CFTR activation in promoting the functional maturation of the premature human intestine.