ArticleJournal of inflammation research2021
The β3/5 Integrin-MMP9 Axis Regulates Pulmonary Inflammatory Response and Endothelial Leakage in Acute Lung Injury.
Article in Journal of inflammation research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Integrated Transcriptomic and Proteomic Analysis of the Pathogenic Mechanisms ofAnimals : an open access journal from MDPI · 2026Article
- Embryo-fetal and early-life protein restriction programs pulmonary structure and molecular parameters in both dams and female offspring.Molecular and cellular biochemistry · 2026Article
- Sex-Specific Pathophysiological Signatures in Allometric Dosing-Controlled Bleomycin Acute Lung Injury Model.bioRxiv : the preprint server for biology · 2026Article
- From Alveolar Injury to Precision Perioperative Care: Integrating Molecular Biomarkers and Technology-Enabled Strategies for Prolonged Air Leak After Lung Resection.Mediators of inflammation · 2026Review
- Sulfonium lipid nanoparticles for intranasal mRNA delivery to lung epithelial and immune cells.Acta biomaterialia · 2025Article
- Increased Kindlin-2 via SMURF1 Inhibition Attenuates Endothelial Permeability and Acute Lung Injury.International journal of molecular sciences · 2025Article
- Chaihuang Qingfu Pills Protect Against Acute Pancreatitis-Associated Acute Lung Injury Through MMP9-NLRP3-Pyroptosis Pathway.Journal of inflammation research · 2025Article
- Acute aortic dissection-induced acute respiratory distress syndrome: pathogenesis and clinical implications.Frontiers in cardiovascular medicine · 2025Review
- Gene expression response to Salmonella Typhimurium in the cecal tonsil reveals a potential mechanism of resistance in chickens.Poultry science · 2024Article
- The prognostic and immune infiltration role of ITGB superfamily members in non-small cell lung cancer.American journal of translational research · 2022Article
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Authors and funding
18 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute lung injury (ALI) is a severe respiratory disease with high rates of morbidity and mortality. Many mediators regarding endogenous or exogenous are involved in the pathophysiology of ALI. Here, we have uncovered the involvement of integrins and matrix metalloproteinases, as critical determinants of excessive inflammation and endothelial permeability, in the regulation of ALI.
methodsInflammatory cytokines were measured by quantitative real-time PCR for mRNA levels and ELISA for secretion levels. Endothelial permeability assay was detected by the passage of rhodamine B isothiocyanate-dextran. Mice lung permeability was assayed by Evans blue albumin (EBA). Western blot was used for protein level measurements. The intracellular reactive oxygen species (ROS) were evaluated using a cell-permeable probe, DCFH-DA. Intratracheal injection of lipopolysaccharide (LPS) into mice was conducted to establish the lung injury model.
resultsExogenous MMP-9 significantly aggravated the inflammatory response and permeability in mouse pulmonary microvascular endothelial cells (PMVECs) treated by LPS, whereas knockdown of MMP-9 exhibited the opposite phenotypes. Knockdown of integrin β3 or β5 in LPS-treated PMVECs significantly downregulated MMP-9 expression and decreased inflammatory response and permeability in the presence or absence of exogenous MMP-9. Additionally, the interaction of MMP-9 and integrin β5 was impaired by a ROS scavenger, which further decreased the pro-inflammatory cytokines production and endothelial leakage in PMVECs subjected to co-treatment (LPS with exogenous MMP-9). In vivo studies, exogenous MMP-9 treatment or knockdown β3 integrin significantly decreased survival in ALI mice. Notably, knockdown of β5 integrin alone had no remarkable effect on survival, but which combined with anti-MMP-9 treatment significantly improved the survival by ameliorating excessive lung inflammation and permeability in ALI mice.
conclusionThese findings support the β3/5 integrin-MMP-9 axis as an endogenous signal that could play a pivotal role in regulating inflammatory response and alveolar-capillary permeability in ALI.
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