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Abstract <p>Damage to the blood–testis barrier (BTB) induced by chemotherapeuticagents is a major cause of spermatogenic dysfunction. Bone marrowmesenchymal stem cell (BMSC)–derived exosomes possess tissue repairpotential, yet their role and mechanism in BTB restoration remainunclear. This study explored whether BMSC exosomes improve BTB injuryand spermatogenic impairment via delivery of microRNA (miR)-34c-5p.For this a cyclophosphamide (CTX)–induced BTB injury model was establishedin Sprague–Dawley rats, which were randomized into five groups (<i>n</i> = 8): normal control (NC), CTXmodel, miR-NC exosome, miR-34c-5p exosome, and miR-34c-5p exosome+ Antagomir. Sperm concentration, motility, and viability were measured;seminiferous tubule morphology and spermatogenesis were evaluatedby HE staining and histological scoring. Expression of BTB tightjunction proteins (Occludin, Claudin-1) and miR-34c-5p levels intesticular tissue were determined by Western blot and RT-qPCR. Thedata obtained demonstrated that CTX markedly reduced sperm parameters,disrupted seminiferous structure, decreased Occludin, Claudin-1,and miR-34c-5p expression. miR-34c-5p exosomes restored sperm quality,improved testicular histology, increased spermatogenic scores, andupregulated Occludin, Claudin-1, and miR-34c-5p; these effects were reversedby miR-34c-5p inhibition. This allowed us to conclude that BMSC-derivedexosomal miR-34c-5p enhances tight junction protein expression, therebymitigating the damage to the BTB and the decline in sperm qualitycaused by CTX, providing a novel therapeutic strategy for male infertilityinvolving exosome- and miRNA-based interventions.</p>

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MicroRNA-34c-5p Cargo in BMSC-Derived Exosomes Alleviates Blood–Testis Barrier Injury—Induced Spermatogenic Deficits

  • 期刊论文

  • 发表日期：

    2026年4月19日

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  • Li Quan,
  • Yanfei Gong,
  • Fang Peng,
  • Qi Li,
  • Gaobo Huang

摘要

Abstract

Damage to the blood–testis barrier (BTB) induced by chemotherapeuticagents is a major cause of spermatogenic dysfunction. Bone marrowmesenchymal stem cell (BMSC)–derived exosomes possess tissue repairpotential, yet their role and mechanism in BTB restoration remainunclear. This study explored whether BMSC exosomes improve BTB injuryand spermatogenic impairment via delivery of microRNA (miR)-34c-5p.For this a cyclophosphamide (CTX)–induced BTB injury model was establishedin Sprague–Dawley rats, which were randomized into five groups (n = 8): normal control (NC), CTXmodel, miR-NC exosome, miR-34c-5p exosome, and miR-34c-5p exosome+ Antagomir. Sperm concentration, motility, and viability were measured;seminiferous tubule morphology and spermatogenesis were evaluatedby HE staining and histological scoring. Expression of BTB tightjunction proteins (Occludin, Claudin-1) and miR-34c-5p levels intesticular tissue were determined by Western blot and RT-qPCR. Thedata obtained demonstrated that CTX markedly reduced sperm parameters,disrupted seminiferous structure, decreased Occludin, Claudin-1,and miR-34c-5p expression. miR-34c-5p exosomes restored sperm quality,improved testicular histology, increased spermatogenic scores, andupregulated Occludin, Claudin-1, and miR-34c-5p; these effects were reversedby miR-34c-5p inhibition. This allowed us to conclude that BMSC-derivedexosomal miR-34c-5p enhances tight junction protein expression, therebymitigating the damage to the BTB and the decline in sperm qualitycaused by CTX, providing a novel therapeutic strategy for male infertilityinvolving exosome- and miRNA-based interventions.