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We began analyzing https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.107.161067, but it redirected us to https://www.ahajournals.org/doi/10.1161/CIRCRESAHA.107.161067. The analysis below is for the second page.

Title[redir]:
Interleukin-1β Causes Acute Lung Injury via αvβ5 and αvβ6 Integrin–Dependent Mechanisms | Circulation Research
Description:
Interleukin (IL)-1β has previously been shown to be among the most biologically active cytokines in the lungs of patients with acute lung injury (ALI). Furthermore, there is experimental evidence that lung vascular permeability increases after short-term exposure to IL-1 protein, although the exact mechanism is unknown. Therefore, the objective of this study was to determine the mechanisms of IL-1β–mediated increase in lung vascular permeability and pulmonary edema following transient overexpression of this cytokine in the lungs by adenoviral gene transfer. Lung vascular permeability increased with intrapulmonary IL-1β production with a maximal effect 7 days after instillation of the adenovirus. Furthermore, inhibition of the αvβ6 integrin and/or transforming growth factor-β attenuated the IL-1β–induced ALI. The results of in vitro studies indicated that IL-1β caused the activation of transforming growth factor-β via RhoA/αvβ6 integrin–dependent mechanisms and the inhibition of the αvβ6 integrin and/or transforming growth factor-β signaling completely blocked the IL-1β–mediated protein permeability across alveolar epithelial cell monolayers. In addition, IL-1β increased protein permeability across lung endothelial cell monolayers via RhoA- and αvβ5 integrin–dependent mechanisms. The final series of in vivo experiments demonstrated that pretreatment with blocking antibodies to both the αvβ5 and αvβ6 integrins had an additive protective effect against IL-1β–induced ALI. In summary, these results demonstrate a critical role for the αvβ5/β6 integrins in mediating the IL-1β–induced ALI and indicate that these integrins could be a potentially attractive therapeutic target in ALI.

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Keywords {🔍}

ilβ, lung, αvβ, permeability, cell, tgfβ, integrin, endothelial, monolayers, increase, cells, crossref, research, figure, vehicle, pubmed, google, scholar, epithelial, protein, blocking, activation, biology, ngml, jfp, department, shown, rhoa, treated, vascular, pulmonary, control, injury, signaling, data, mechanisms, results, mice, ali, receptor, acute, view, exposure, edema, increased, ilβmediated, atii, pretreated, paracellular, medicine,

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aha/asa scientific statements supplemental material file author jean-françois pittet gram-negative bacteria–derived endotoxin gram-negative–derived lipopolysaccharide belong jean-françois pittet american heart association rhoa/αvβ6 integrin/tgf-β pathway rhoa/αvβ6-dependent tgf-β activation transforming growth factor-β αvβ6 integrin/tgf-β pathway author jérémie roux interleukin-1beta decreases expression il-1β–mediated increased permeability il-1β activate tgf-β αvβ6-dependent tgf-β activation ad-hil-1β intratracheal instillation il-1β–mediated protein permeability heart failure stroke activates tgf-β signaling il-1β–mediated lung edema rhoa/αvβ6 integrin–dependent mechanisms tgf-β signaling inhibits platelet-activating factor contributes rhoa/αvβ6 integrin–dependent mechanism ventilator-induced lung injury submit tumor necrosis factor-α tgf-β cell signaling mediating il-1β–induced increase latent inactive tgf-β red ™ aha tgf-β–dependent mechanisms cytokine-induced neutrophil chemoattractant-1 cytokine-induced neutrophil chemoattractant il-1β signaling pathway jérémie roux measure active tgf-β active mature tgf-β mechanisms activate tgf-β expressing human il-1β main content advertisement αvβ6 integrin–dependent manner il-1beta-dependent mechanism receptor antagonist il-1ra acknowledgments sources authors contributed equally international users arteriosclerosis na+-driven fluid transport hil-1β–mediated increase

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Does IL-1β activate TGF-β via the αvβ6 integrin pathway?
What are the mechanisms of TGF-β activation in the lungs?

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