ArticlePloS one2015
Mononuclear Phagocyte-Derived Microparticulate Caspase-1 Induces Pulmonary Vascular Endothelial Cell Injury.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed.
- Extracellular Vesicles as Drivers of Lung Endothelial Dysfunction in ARDS: Mechanisms and Therapeutic Opportunities.Comprehensive Physiology · 2026Review
- Quantifying pathway perturbations based on gene network rewiring in sepsis progression toward death or survival.Frontiers in bioinformatics · 2026Article
- ApoA1/HDL and sepsis-associated vascular endothelial injury: a narrative review.Critical care (London, England) · 2025Review
- Caspases help to spread the message via extracellular vesicles.The FEBS journal · 2023Review
- Regulation of Mesenchymal Cell Fate by Transfer of Active Gasdermin-D via Monocyte-Derived Extracellular Vesicles.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- LAMP3 transfer via extracellular particles induces apoptosis in Sjögren's disease.Scientific reports · 2023Article
- Extracellular Vesicles in Sepsis: Pathogenic Roles, Organ Damage, and Therapeutic Implications.International journal of medical sciences · 2023Review
- Interactions between the NLRP3-Dependent IL-1β and the Type I Interferon Pathways in Human Plasmacytoid Dendritic Cells.International journal of molecular sciences · 2022Article
- Extracellular vesicles participate in the pathogenesis of sepsis.Frontiers in cellular and infection microbiology · 2022Review
- The Connection Between Selected Caspases Levels in Bronchoalveolar Lavage Fluid and Severity After Brain Injury.Frontiers in neurology · 2022Article
- Size Distribution of Microparticles: A New Parameter to Predict Acute Lung Injury After Cardiac Surgery With Cardiopulmonary Bypass.Frontiers in cardiovascular medicine · 2022Article
- Review
- The potential involvement of P2X7 receptor in COVID-19 pathogenesis: A new therapeutic target?Scandinavian journal of immunology · 2021Review
- Inflammatory Caspases Drive Pyroptosis in Acute Lung Injury.Frontiers in pharmacology · 2021Review
- Extracellular Vesicles and Alveolar Epithelial-Capillary Barrier Disruption in Acute Respiratory Distress Syndrome: Pathophysiological Role and Therapeutic Potential.Frontiers in physiology · 2021Review
- Intracellular and Extracellular Lipopolysaccharide Signaling in Sepsis: Avenues for Novel Therapeutic Strategies.Journal of innate immunity · 2021Review
- The protective effects of C16 peptide and angiopoietin-1 compound in lipopolysaccharide-induced acute respiratory distress syndrome.Experimental biology and medicine (Maywood, N.J.) · 2020Article
- Extracellular vesicles: novel communicators in lung diseases.Respiratory research · 2020Review
- Exosomes in Sepsis.Frontiers in immunology · 2020Review
- Prdx4 limits caspase-1 activation and restricts inflammasome-mediated signaling by extracellular vesicles.The EMBO journal · 2019Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Lung endothelial cell apoptosis and injury occurs throughout all stages of acute lung injury (ALI/ARDS) and impacts disease progression. Lung endothelial injury has traditionally been focused on the role of neutrophil trafficking to lung vascular integrin receptors induced by proinflammatory cytokine expression. Although much is known about the pathogenesis of cell injury and death in ALI/ARDS, gaps remain in our knowledge; as a result of which there is currently no effective pharmacologic therapy. Enzymes known as caspases are essential for completion of the apoptotic program and secretion of pro-inflammatory cytokines. We hypothesized that caspase-1 may serve as a key regulator of human pulmonary microvascular endothelial cell (HPMVEC) apoptosis in ALI/ARDS. Our recent experiments confirm that microparticles released from stimulated monocytic cells (THP1) induce lung endothelial cell apoptosis. Microparticles pretreated with the caspase-1 inhibitor, YVAD, or pan-caspase inhibitor, ZVAD, were unable to induce cell death of HPMVEC, suggesting the role of caspase-1 or its substrate in the induction of HPMVEC cell death. Neither un-induced microparticles (control) nor direct treatment with LPS induced apoptosis of HPMVEC. Further experiments showed that caspase-1 uptake into HPMVEC and the induction of HPMVEC apoptosis was facilitated by caspase-1 interactions with microparticulate vesicles. Altering vesicle integrity completely abrogated apoptosis of HPMVEC suggesting an encapsulation requirement for target cell uptake of active caspase-1. Taken together, we confirm that microparticle centered caspase-1 can play a regulator role in endothelial cell injury.
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