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ORIGINAL RESEARCH article

Front. Pediatr.
Sec. Pediatric Pulmonology
Volume 12 - 2024 | doi: 10.3389/fped.2024.1295868

Hyperoxia exposure promotes endothelial-mesenchymal transition and inhibits regulatory T cell function in human pulmonary microvascular endothelial cells

Provisionally accepted
Yifan Sun Yifan Sun Chongbing Yan Chongbing Yan Yibo Liu Yibo Liu Yating Lin Yating Lin Bowen Weng Bowen Weng Xiaohui Gong Xiaohui Gong Cheng Cai Cheng Cai *
  • Shanghai Children's Hospital, Shanghai, Shanghai Municipality, China

The final, formatted version of the article will be published soon.

    Objective: This study aims to investigate the effects of hyperoxia exposure on TGF-β1-induced endothelial-mesenchymal transition (EndoMT) and regulatory T cell (Treg) - mediated immunomodulation in human pulmonary microvascular endothelial cells (HPMECs), which could provide a theoretical basis for further studies of the pathogenesis of bronchopulmonary dysplasia (BPD). Methods: A BPD cell model was established by exposing HPMECs to hyperoxia. Flow cytometry was used to isolate CD4+CD3+CD25 +CD127- Tregs from the peripheral blood samples of preterm infants. HPMECs were divided into four groups based on whether they were exposed to hyperoxia and/or co-cultured with Tregs. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were used to test the expression levels of TGF-β1, α-SMA, Foxp3, IL-10, and reactive oxygen species (ROS). Results: The results showed that the expression levels of TGF-β1 and α-SMA in HPMECs increased at 24h, 48h, and 72h of hyperoxia exposure. In the co-culture group of HPMECs and Tregs, Foxp3 and IL-10 expressions decreased at 48h and 72h of hyperoxia exposure. ROS expression increased in the hyperoxia group of HPMECs at 24h, 48h, and 72h of hyperoxia exposure, which were higher than those in the hyperoxia group of HPMECs and Tregs. Conclusion: These findings suggest that hyperoxia exposure promotes EndoMT in HMPECs and inhibits the immunosuppressive effect of Tregs. Despite this, Tregs still seem could protect HPMECs from oxidative stress injury.

    Keywords: Regulatory T Cell, Endothelial-mesenchymal transition, Human pulmonary microvascular endothelial cell, Hyperoxia exposure, Bronchopulmonary Dysplasia

    Received: 17 Sep 2023; Accepted: 04 Jul 2024.

    Copyright: © 2024 Sun, Yan, Liu, Lin, Weng, Gong and Cai. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence: Cheng Cai, Shanghai Children's Hospital, Shanghai, 200062, Shanghai Municipality, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.