ArticleInternational journal of molecular sciences2019
Differential Protein Expression Profiles of Bronchoalveolar Lavage Fluid Following Lipopolysaccharide-Induced Direct and Indirect Lung Injury in Mice.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 30 citations in OpenAlex.
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- Longitudinal proteomic analysis of pathophysiology in plasma and bronchoalveolar lavage fluid of patients with ARDS.Journal of intensive care · 2025Article
- UBR1 Promotes Sex-Dependent ACE2 Ubiquitination in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2025Article
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- Mitochondrial transplantation attenuates lipopolysaccharide-induced acute respiratory distress syndrome.BMC pulmonary medicine · 2024Article
- Serotonin-2 Receptor Agonists Produce Anti-inflammatory Effects through Functionally Selective Mechanisms That Involve the Suppression of Disease-Induced Arginase 1 Expression.ACS pharmacology & translational science · 2024Article
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- Reactive Oxygen Species and Strategies for Antioxidant Intervention in Acute Respiratory Distress Syndrome.Antioxidants (Basel, Switzerland) · 2023Review
- Personalized medicine using omics approaches in acute respiratory distress syndrome to identify biological phenotypes.Respiratory research · 2022Review
- Tumor Progression Locus 2 Protects against Acute Respiratory Distress Syndrome in Influenza A Virus-Infected Mice.Microbiology spectrum · 2022Article
- Proteomic and Bioinformatics Analysis of Membrane Lipid Domains after Brij 98 Solubilization of Uninduced and Phenobarbital-Induced Rat Liver Microsomes: Defining the Membrane Localization of the P450 Enzyme System.Drug metabolism and disposition: the biological fate of chemicals · 2022Article
- Isoorientin suppresses sepsis-induced acute lung injury in mice by activating an EPCR-dependent JAK2/STAT3 pathway.Journal of molecular histology · 2022Article
- Exploration of the Potential Link, Hub Genes, and Potential Drugs for Coronavirus Disease 2019 and Lung Cancer Based on Bioinformatics Analysis.Journal of oncology · 2022Article
- Chronic binge alcohol and ovariectomy dysregulate omental adipose tissue metaboproteome in simian immunodeficiency virus-infected female macaques.Physiological genomics · 2021Article
- Non-targeted proteomics of acute respiratory distress syndrome: clinical and research applications.Proteome science · 2021Review
- Lrp1 Regulation of Pulmonary Function. Follow-Up of Human GWAS in Mice.American journal of respiratory cell and molecular biology · 2021Article
- Host mitochondrial transcriptome response to SARS-CoV-2 in multiple cell models and clinical samples.Scientific reports · 2021Article
- Mobilization of Iron Stored in Bacterioferritin Is Required for Metabolic Homeostasis inPathogens (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The pathogenic mechanisms of acute lung injury due to direct and indirect pulmonary insults are incompletely understood. Using an unbiased, discovery and quantitative proteomic approach, we examined bronchoalveolar lavage fluid (BALF) proteome following lipopolysaccharide (LPS)-induced direct and indirect lung injury in mice. A total of 1017 proteins were both identified and quantitated in BALF from control, intratracheal (I.T., direct) and intraperitoneal (I.P., indirect) LPS-treated mice. The two LPS groups shared 13 up-regulated and 22 down-regulated proteins compared to the control group. Ingenuity pathway analysis revealed that acute-phase response signaling was activated by both I.T. and I.P. LPS; however, the magnitude of activation was much greater in the I.T. LPS group. Intriguingly, two canonical signaling pathways, liver X receptor/retinoid X receptor activation, and the production of nitric oxide and reactive oxygen species in macrophages, were activated by I.T. but suppressed by I.P. LPS. Cxcl15 (also known as lungkine) was also up-regulated by I.T. but down-regulated by I.P. LPS. In conclusion, our quantitative discovery-based proteomic approach identified commonalities, as well as significant differences in BALF protein expression profiles between LPS-induced direct and indirect lung injury, and importantly, LPS-induced indirect lung injury resulted in suppression of select components of lung innate immunity.
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