AI Article Synopsis

  • Oxygen deprivation and excess are both toxic, making the body's adaptation to oxygen levels crucial for survival.
  • The study investigates protein turnover rates in mouse heart, lung, and brain under different oxygen levels, finding that the lung shows the most significant response.
  • It highlights that certain extracellular matrix proteins stabilize in the lung during both low (hypoxia) and high (hyperoxia) oxygen, while a component of the electron transport chain becomes unstable in high oxygen, implicating MYBBP1A as a regulator in this context.

Article Abstract

Oxygen deprivation and excess are both toxic. Thus, the body's ability to adapt to varying oxygen tensions is critical for survival. While the hypoxia transcriptional response has been well studied, the post-translational effects of oxygen have been underexplored. In this study, we systematically investigate protein turnover rates in mouse heart, lung, and brain under different inhaled oxygen tensions. We find that the lung proteome is the most responsive to varying oxygen tensions. In particular, several extracellular matrix (ECM) proteins are stabilized in the lung under both hypoxia and hyperoxia. Furthermore, we show that complex 1 of the electron transport chain is destabilized in hyperoxia, in accordance with the exacerbation of associated disease models by hyperoxia and rescue by hypoxia. Moreover, we nominate MYBBP1A as a hyperoxia transcriptional regulator, particularly in the context of rRNA homeostasis. Overall, our study highlights the importance of varying oxygen tensions on protein turnover rates and identifies tissue-specific mediators of oxygen-dependent responses.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10708181PMC
http://dx.doi.org/10.1126/sciadv.adj4884DOI Listing

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