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Deubiquitinase USP2 accelerates endothelial glycocalyx degradation in sepsis-induced lung injury

ABSTRACT: Sepsis-induced acute lung injury is characterized by severe pulmonary endothelial dysfunction and endothelial glycocalyx degradation. To investigate the molecular mechanisms underlying ubiquitin-specific protease 2 (USP2)-mediated endothelial injury, immunoprecipitation coupled with liquid chromatography-tandem mass spectrometry (IP-MS) was performed to identify proteins associated with USP2. Human umbilical vein endothelial cells (HUVECs) overexpressing USP2 were subjected to immunoprecipitation using anti-Flag antibodies, and the resulting protein complexes were analyzed by LC-MS/MS. Candidate interacting proteins were identified through comparative proteomic analysis and further prioritized based on subcellular localization and biological function. This dataset was generated to characterize the USP2 interactome and facilitate the identification of downstream effectors involved in endothelial glycocalyx regulation during sepsis. The mass spectrometry data support a study investigating the role of USP2 in pulmonary endothelial injury and reveal mitochondrial carrier homolog 2 (MTCH2) as a candidate USP2-associated protein. Raw mass spectrometry files and processed identification results are provided to enable data reuse and independent validation.

ORGANISM(S): Homo Sapiens

SUBMITTER: Fengmei Guo

PROVIDER: PXD080141 | iProX | Tue Jun 23 00:00:00 BST 2026

REPOSITORIES: iProX

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Project description:Sepsis is the most common cause of hospitalization worldwide. Millions of people survive sepsis each year and are at risk for rehospitalization and death. Pulmonary complications such as respiratory failure due to pneumonia and exacerbation of chronic respiratory disease are among the most common reasons for rehospitalization in sepsis survivors. In order to prevent additional morbidity and death in patients surviving sepsis, we must establish biomarkers to identify patients at risk for pulmonary complications and develop treatments. Late complications in sepsis survivors, particularly nosocomial infections, are proposed to occur through persistent immune reprogramming after sepsis known as immunoparalysis. However, pro-inflammatory immune reprogramming in the form of primed or enhanced responses to secondary stimuli has also been described and could directly contribute to tissue injury and death. Primed immune responses and their contribution to long-term sepsis complications remains understudied. We hypothesize that primed immune responses to inflammatory stimuli in the lung after sepsis are associated with pulmonary complications in survivors of sepsis. To this end, we developed a model of antibiotic treated sepsis induced by cecal ligation and puncture followed three weeks later by secondary challenge with intranasal lipopolysaccharide to induce inflammatory lung injury. We find that mice surviving sepsis have enhanced lung injury responses in the setting of an exaggerated proinflammatory immune response, including primed Ly6Chi monocyte Tnf expression. Using RNA sequencing, we identified derangements in lung gene expression after CLP prior to LPS administration which may mediate enhanced lung injury in this model. One potential mediator, S100A8/A9, was also found to be elevated in the circulation of human sepsis survivors for up to 180 days after sepsis. These findings validate our model and identify S100A8/A9 as one of many potential biomarkers and therapeutic targets for patients at risk for long-term pulmonary complications after sepsis. The role of S100A8/A9, monocyte priming, and other factors predisposing to enhanced lung injury responses and pulmonary complications after sepsis warrant further investigation in humans and mice.

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Deubiquitinase USP2 accelerates endothelial glycocalyx degradation in sepsis-induced lung injury

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