Upregulation of the tight junction protein occludin: effects on ventilation-induced lung injury and mechanisms of action

Liu, Mengjie; Gu, Chao; Wang, Yuelan

doi:10.1186/1471-2466-14-94

Cited by 43 publications

(41 citation statements)

References 20 publications

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“…In addition, the higher levels of total proteins induced by LPS in BALF were also inhibited by PIC treatment. Furthermore, tight junction proteins serve as important components in keeping the permeability of the air-blood barrier, and are down-regulated in the lung during ALI (Herold et al, 2013;Liu et al, 2014). In our study, we also found that the expression of tight junction protein ZO-1 and occludin were significantly reduced in the LPS treatment group mice compared to that in the control groups mice.…”

Section: Discussionsupporting

confidence: 74%

Protective Effect of Piceatannol Against Acute Lung Injury Through Protecting the Integrity of Air-Blood Barrier and Modulating the TLR4/NF-κB Signaling Pathway Activation

et al. 2020

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Acute lung injury (ALI) is a common and complex inflammatory lung syndrome with higher morbidity and mortality rate. Piceatannol (PIC) has anti-inflammation and anti-oxidant properties. The study was designed to explore the effect and the action mechanisms of PIC on lipopolysaccharide (LPS)-induced ALI. Twenty-four hours after LPS challenge, mice from different treatment groups were euthanized, and the bronchoalveolar lavage fluid (BALF) and lung tissue samples were collected. Then the degree of pulmonary edema, lung pathological changes, myeloperoxidase (MPO) activity, and the production of pro-inflammatory cytokines were detected. Additionally, the messenger RNA (mRNA) expressions associated with cell adhesion molecules and tight junction were analyzed through quantitative real-time (qRT)-PCR, and the TLR4/NF-kB activation was examined by western blot. The results showed that PIC significantly inhibited LPS-induced lung edema, histopathological damage, MPO activity, cell infiltration, and pro-inflammatory cytokines production. Moreover, PIC notably suppressed mRNA expressions associated with inflammation and cell adhesion molecules. Furthermore, PIC also alleviated LPSinduced damage of air-blood barrier through reducing the levels of total proteins in BALF and recovering the expression of occludin and ZO-1 in the lung tissues. We also found that PIC remarkably restrained the LPS-induced TLR4/NF-kB pathway activation in lung tissues. In conclusion, PIC may be potential to treat LPS-induced acute lung injury (ALI) via regulating air-blood barrier and TLR4/NF-kB signaling pathway activation.

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Section: Discussionsupporting

confidence: 74%

Protective Effect of Piceatannol Against Acute Lung Injury Through Protecting the Integrity of Air-Blood Barrier and Modulating the TLR4/NF-κB Signaling Pathway Activation

et al. 2020

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“…Regarding connexin 43, the data in the literature are controversial. While some studies showed increased expression of connexin 43 following ALI/ARDS (21,26), others reported an absence of connexin 43 within a few days after exposure to endotoxin (17). Unlike VE-cadherin, claudin 18 and 5, and connexin 43, in our hands, occludin levels failed to show a sign of decline at early time points after exposure to ricin, their reduction being observed…”

Section: L264contrasting

confidence: 78%

“…only from 48 h postexposure onwards. Decreased levels of occludin were documented by others in ventilation-induced lung injury (21). Neutrophils are proposed to have an important role in mediating ALI/ARDS.…”

Section: L265mentioning

confidence: 82%

Early disruption of the alveolar-capillary barrier in a ricin-induced ARDS mouse model: neutrophil-dependent and -independent impairment of junction proteins

Sapoznikov

Gal

Falach

et al. 2019

American Journal of Physiology-Lung Cellular and Molecular Phys

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Irrespective of its diverse etiologies, acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) leads to increased permeability of the alveolar-capillary barrier, which in turn promotes edema formation and respiratory failure. We investigated the mechanism of ALI/ARDS lung hyperpermeability triggered by pulmonary exposure of mice to the highly toxic plant-derived toxin ricin. One prominent hallmark of ricin-mediated pulmonary intoxication is the rapid and massive influx of neutrophils to the lungs, where they contribute to the developing inflammation yet may also cause tissue damage, thereby promoting ricin-mediated morbidity. Here we show that pulmonary exposure of mice to ricin results in the rapid diminution of the junction proteins VE-cadherin, claudin 5, and connexin 43, belonging, respectively, to the adherens, tight, and gap junction protein families. Depletion of neutrophils in ricin-intoxicated mice attenuated the damage caused to these junction proteins, alleviated pulmonary edema, and significantly postponed the time to death of the intoxicated mice. Inhibition of matrix metalloproteinase (MMP) activity recapitulated the response to neutrophil depletion observed in ricin-intoxicated mice and was associated with decreased insult to the junction proteins and alveolar-capillary barrier. However, neutrophil-mediated MMP activity was not the sole mechanism responsible for pulmonary hyperpermeability, as exemplified by the ricin-mediated disruption of claudin 18, via a neutrophil-independent mechanism involving tyrosine phosphorylation. This in-depth study of the early stage mechanisms governing pulmonary tissue integrity during ALI/ARDS is expected to facilitate the tailoring of novel therapeutic approaches for the treatment of these diseases.

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“…Consistent with a role in regulating paracellular permeability, decreased lung occludin has been associated with several conditions known to promote pulmonary edema, including exposure to environmental toxicants, ventilator induced lung injury (VILI) and chronic exposure to alcohol [60–64]. Also, rats pretreated with a PKCα inhibitor (bisindolylmaleimide) were protected from VILI, which correlated with an increase in total lung occludin protein [65]. Whether diminished occludin expression associated with VILI has an effect on claudins was not determined nor was it determined whether occludin was necessary for protection from VILI.…”

Section: Claudin Structure and Composition In Tight Junctionsmentioning

confidence: 99%

Claudins: Gatekeepers of lung epithelial function

Schlingmann

Molina

Koval

2015

Seminars in Cell & Developmental Biology

155

108

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The lung must maintain a proper barrier between airspaces and fluid filled tissues in order to maintain lung fluid balance. Central to maintaining lung fluid balance are epithelial cells which create a barrier to water and solutes. The barrier function of these cells is mainly provided by tight junction proteins known as claudins. Epithelial barrier function varies depending on the different needs within the segments of the respiratory tree. In the lower airways, fluid is required to maintain mucociliary clearance, whereas in the terminal alveolar airspaces a thin layer of surfactant enriched fluid lowers surface tension to prevent airspace collapse and is critical for gas exchange. As the epithelial cells within the segments of the respiratory tree differ, the composition of claudins found in these epithelial cells is also different. Among these differences is claudin-18 which is uniquely expressed by the alveolar epithelial cells. Other claudins, notably claudin-4 and claudin-7, are more ubiquitously expressed throughout the respiratory epithelium. Claudin-5 is expressed by both pulmonary epithelial and endothelial cells. Based on in vitro and in vivo model systems and histologic analysis of lungs from human patients, roles for specific claudins in maintaining barrier function and protecting the lung from the effects of acute injury and disease are being identified. One surprising finding is that claudin-18 and claudin-4 control lung cell phenotype and inflammation beyond simply maintaining a selective paracellular permeability barrier. This suggests claudins have more nuanced roles for the control of airway and alveolar physiology in the healthy and diseased lung.

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Upregulation of the tight junction protein occludin: effects on ventilation-induced lung injury and mechanisms of action

Cited by 43 publications

References 20 publications

Protective Effect of Piceatannol Against Acute Lung Injury Through Protecting the Integrity of Air-Blood Barrier and Modulating the TLR4/NF-κB Signaling Pathway Activation

Protective Effect of Piceatannol Against Acute Lung Injury Through Protecting the Integrity of Air-Blood Barrier and Modulating the TLR4/NF-κB Signaling Pathway Activation

Early disruption of the alveolar-capillary barrier in a ricin-induced ARDS mouse model: neutrophil-dependent and -independent impairment of junction proteins

Claudins: Gatekeepers of lung epithelial function

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