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ORIGINAL RESEARCH article

Front. Physiol.

Sec. Redox Physiology

Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice

Provisionally accepted
Ramani SoundararajanRamani Soundararajan1Sahebgowda Sidramagowda PatilSahebgowda Sidramagowda Patil2Mason T. BreitzigMason T. Breitzig3Matthew AlleynMatthew Alleyn4Venkata Ramireddy NaralaVenkata Ramireddy Narala5Lakshmi GalamLakshmi Galam4Richard LockeyRichard Lockey4Narasaiah KolliputiNarasaiah Kolliputi4*
  • 1Morsani College of Medicine Surgery, University of South Florida, Tampa, FL, United States
  • 2The University of Iowa Department of Anatomy and Cell Biology, Iowa City, United States
  • 3Henry Ford Health System, Detroit, United States
  • 4Internal Medicine/Allergy and Immunology, University of South Florida, Tampa, FL, United States
  • 5Yogi Vemana University, Kadapa, India

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Administering high levels of oxygen is a life-sustaining measure in critically ill lung subjects. However, prolonged hyperoxia exposure increases reactive oxygen species (ROS) that exacerbate oxidative stress, mitochondrial dysfunction, respiratory failure and cell death. Mitochondria play a critical role in hyperoxia-induced acute lung injury (HALI). The specific role of the Polycomb Repressive Complex 1 protein BMI1 (B cell-specific Moloney murine leukemia virus integration site 1) in mitochondrial damage remains unknown. Bmi1 knockout mice (Bmi1-/-) and their wild-type (WT) littermates were exposed to normobaric hyperoxia using oxygen concentrations of 95-100% for 48h to assess BMI1 function in HALI. Mice lacking Bmi1 versus WT exposed to hyperoxia exhibited hallmarks of human acute lung injury (ALI) such as increased lung permeability, alveolar edema, hemorrhage, interstitial thickening, and infiltration of immune cells; and alterations in lung mechanics, including increased elastance and decreased lung compliance. Bmi1-/- mice exhibit increased mitochondrial damage, increased oxidative stress, and significant changes in protein markers related to mitophagy compared to WT mice. Our results indicate that Bmi1-/- mice are susceptible to HALI and the damage increases in those mice compared with their WT littermates.

Keywords: BMI1, Hali, Hyperoxia-induced acute lung injury, mitochondr ia, ARDS (acute respiratory disease syndrome)

Received: 08 Sep 2025; Accepted: 27 Oct 2025.

Copyright: © 2025 Soundararajan, Patil, Breitzig, Alleyn, Narala, Galam, Lockey and Kolliputi. 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: Narasaiah Kolliputi, nkollipu@usf.edu

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.

Supplementary Material