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<p>Endogenous retroviruses (ERVs) are genetic elements derived from a process of germline infection by exogenous retroviruses. Some ERVs have been co-opted for physiological functions, and their activation has been associated with complex diseases, including Autism Spectrum Disorder (ASD). We have already demonstrated an abnormal expression of ERVs in the BTBR T + tf/J (BTBR) mouse model of ASD during intrauterine life till adulthood. Thus, starting from the assumptions that ERVs may contribute to the derailment of neurodevelopment and that ASD has fetal origins as a consequence of adverse intrauterine conditions, the present study aims to characterize the transcriptional activity of selected ERVs (MusD, IAP, Syn-A, Syn-B, ARC and GLN), LINE-1, inflammatory mediators (IL-6, IL-10, IL-11 CXCL-1) at the maternal–fetal interface and in dissected embryos from BTBR mice. Our results highlight the deregulation of ERVs and inflammatory mediators at the maternal–fetal interface, and in cephalic and non-cephalic embryonic tissues from BTBR compared to C57BL/6&#xa0;J. Several correlations among ERV expression levels emerged in different tissues from C57BL/6&#xa0;J mice while, in BTBR mice, no correlations were found, suggesting that in this model, the acquisition of autistic-like traits might be linked to the dysregulation of ERV activity occurring during intra-uterine life.</p>

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Activation of endogenous retroviruses characterizes the maternal-fetal interface in the BTBR mouse model of autism spectrum disorder

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月10日

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  • Chiara Cipriani,
  • Antonella Camaioni,
  • Anna Maria Tartaglione,
  • Martina Giudice,
  • Allegra Conti,
  • Vita Petrone,
  • Martino Tony Miele,
  • Claudia Matteucci,
  • Enrico Garaci,
  • Gemma Calamandrei,
  • Nicola Toschi,
  • Paola Sinibaldi-Vallebona,
  • Laura Ricceri,
  • Emanuela Balestrieri

摘要

Endogenous retroviruses (ERVs) are genetic elements derived from a process of germline infection by exogenous retroviruses. Some ERVs have been co-opted for physiological functions, and their activation has been associated with complex diseases, including Autism Spectrum Disorder (ASD). We have already demonstrated an abnormal expression of ERVs in the BTBR T + tf/J (BTBR) mouse model of ASD during intrauterine life till adulthood. Thus, starting from the assumptions that ERVs may contribute to the derailment of neurodevelopment and that ASD has fetal origins as a consequence of adverse intrauterine conditions, the present study aims to characterize the transcriptional activity of selected ERVs (MusD, IAP, Syn-A, Syn-B, ARC and GLN), LINE-1, inflammatory mediators (IL-6, IL-10, IL-11 CXCL-1) at the maternal–fetal interface and in dissected embryos from BTBR mice. Our results highlight the deregulation of ERVs and inflammatory mediators at the maternal–fetal interface, and in cephalic and non-cephalic embryonic tissues from BTBR compared to C57BL/6 J. Several correlations among ERV expression levels emerged in different tissues from C57BL/6 J mice while, in BTBR mice, no correlations were found, suggesting that in this model, the acquisition of autistic-like traits might be linked to the dysregulation of ERV activity occurring during intra-uterine life.