Control of lung vascular permeability and endotoxin-induced pulmonary oedema by changes in extracellular matrix mechanics

Mammoto, Akiko; Mammoto, Tadanori; Kanapathipillai, Mathumai; Yung, Chong Wing; Jiang, Elisabeth; Jiang, Amanda; Lofgren, Kristopher A.; Gee, Elaine P.S.; Ingber, Donald E.

doi:10.1038/ncomms2774

Cited by 120 publications

(144 citation statements)

References 59 publications

(95 reference statements)

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“…42,43 Administration of LOX and LOXL1-4 inhibitor β-aminopropionitrile [44][45][46] to mice downregulates LOX enzymatic activity and consequently leads to a decrease in lung stiffness. 41 Our previous report demonstrated that periostin regulates LOX enzymatic activity, especially LOX and LOXL1, via BMP-1 activation. 30 While LOXL4 is dominantly expressed in the intact lung, LOX and LOXL1 are also weakly observed.…”

Section: Discussionmentioning

confidence: 99%

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Periostin Deficiency Causes Severe and Lethal Lung Injury in Mice With Bleomycin Administration

Kondoh

Nishiyama

Kikuchi

et al. 2016

J Histochem Cytochem.

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SummaryPulmonary capillary leakage followed by influx of blood fluid into the air space of lung alveoli is a crucial step in the progression of acute lung injury (ALI). This influx is due to increased permeability of the alveolar -capillary barrier. The extracellular matrix (ECM) between the capillary and the epithelium would be expected to be involved in prevention of the influx; however, the role of the ECM remains to be addressed. Here, we show that the ECM architecture organized by periostin, a matricellular protein, plays a pivotal role in the survival of bleomycin-exposed mice. Periostin was localized in the alveolar walls. Although periostin-null mice displayed no significant difference in lung histology and air -blood permeability, they exhibited early lethality in a model of bleomycin-induced lung injury, compared with their wild-type counterparts. This early lethality may have been due to increased pulmonary leakage of blood fluid into the air space in the bleomycin-exposed periostin-null mice. These results suggest that periostin in the ECM architecture prevents pulmonary leakage of blood fluid, thus increasing the survival rate in mice with ALI. Thus, this study provides an evidence for the protective role of the ECM architecture in the lung alveoli. (J Histochem Cytochem 64:441 -453, 2016)

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Section: Discussionmentioning

confidence: 99%

“…41 The LOX superfamily consists of LOX and LOX-like 1 to 4 (LOXL1-4), and all LOXs are capable of initiating collagen cross-linking. 42,43 Administration of LOX and LOXL1-4 inhibitor β-aminopropionitrile [44][45][46] to mice downregulates LOX enzymatic activity and consequently leads to a decrease in lung stiffness.…”

Section: Discussionmentioning

confidence: 99%

Periostin Deficiency Causes Severe and Lethal Lung Injury in Mice With Bleomycin Administration

Kondoh

Nishiyama

Kikuchi

et al. 2016

J Histochem Cytochem.

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“…Monolayer junction formation was analyzed using a confocal Leica SP2 microscope (Leica, Buffalo Grove, IL) (15,20). Endothelial cell permeability was determined by measuring leakage of FITC-labeled BSA (Sigma) through the monolayer of L-HMVE cells, as described previously (13,15).…”

Section: Cell Analysis Methodsmentioning

confidence: 99%

“…L-HMVE cells were cultured for 12 hours and immunostaining was performed with VEcadherin antibody (13,15,20). Monolayer junction formation was analyzed using a confocal Leica SP2 microscope (Leica, Buffalo Grove, IL) (15,20).…”

Section: Cell Analysis Methodsmentioning

confidence: 99%

“…Mice (8-12 wk old) were treated with LPS (2.5 mg/kg, intraperitoneal) and lung vascular permeability was assessed 24 hours after injection (13,15,20). The lung vascular permeability was measured using Evans blue dye or low-molecular weight (LMW), fluorescently labeled dextran (MW 4,000; sigma) leakage (13,15,20).…”

Section: In Vivo Pulmonary Vascular Permeability Assaymentioning

confidence: 99%

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Platelet-Rich Plasma Extract Prevents Pulmonary Edema through Angiopoietin-Tie2 Signaling

Mammoto

Jiang

et al. 2015

Am J Respir Cell Mol Biol

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Increased vascular permeability contributes to life-threatening pathological conditions, such as acute respiratory distress syndrome. Current treatments for sepsis-induced pulmonary edema rely on low-tidal volume mechanical ventilation, fluid management, and pharmacological use of a single angiogenic or chemical factor with antipermeability activity. However, it is becoming clear that a combination of multiple angiogenic/chemical factors rather than a single factor is required for maintaining stable and functional blood vessels. We have demonstrated that mouse platelet-rich plasma (PRP) extract contains abundant angiopoietin (Ang) 1 and multiple other factors (e.g., platelet-derived growth factor), which potentially stabilize vascular integrity. Here, we show that PRP extract increases tyrosine phosphorylation levels of Tunica internal endothelial cell kinase (Tie2) and attenuates disruption of cell-cell junctional integrity induced by inflammatory cytokine in cultured human microvascular endothelial cells. Systemic injection of PRP extract also increases Tie2 phosphorylation in mouse lung and prevents endotoxin-induced pulmonary edema and the consequent decreases in lung compliance and exercise intolerance resulting from endotoxin challenge. Soluble Tie2 receptor, which inhibits Ang-Tie2 signaling, suppresses the ability of PRP extract to inhibit pulmonary edema in mouse lung. These results suggest that PRP extract prevents endotoxin-induced pulmonary edema mainly through Ang-Tie2 signaling, and PRP extract could be a potential therapeutic strategy for sepsis-induced pulmonary edema and various lung diseases caused by abnormal vascular permeability.

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Retraction: Endothelial cell‐specific deficiency of the adenosine deaminase ADAR1 aggravates LPS‐induced lung injury in mice via an MDA5‐independent pathway

et al. 2020

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Adenosine deaminase acting on RNA 1 (ADAR1) has been shown to participate in the regulation of endothelial cells (ECs), as well as local and systemic inflammatory responses. Here, we find that bacterial lipopolysaccharide (LPS)-induced upregulation of ADAR1 in lung ECs is impaired in aged mice, an animal model with high rates of sepsis and mortality. Endothelial cellspecific ADAR1 knockout (ADAR1 ECKO) mice suffer from higher mortality rates, aggravated lung injury, and increased vascular permeability under LPS challenge. In primary ADAR1 knockout ECs, expression of the melanoma differentiation-associated gene 5 (MDA5), a downstream effector of ADAR1, is significantly elevated. MDA5 knockout completely rescues the postnatal offspring death of ADAR1 ECKO mice. However, there is no reduction in mortality or apoptosis in lung cells of ADAR1 ECKO /MDA5 À/À mice challenged with LPS, indicating the involvement of an MDA5-independent mechanism in this process.

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Control of lung vascular permeability and endotoxin-induced pulmonary oedema by changes in extracellular matrix mechanics

Cited by 120 publications

References 59 publications

Periostin Deficiency Causes Severe and Lethal Lung Injury in Mice With Bleomycin Administration

Periostin Deficiency Causes Severe and Lethal Lung Injury in Mice With Bleomycin Administration

Platelet-Rich Plasma Extract Prevents Pulmonary Edema through Angiopoietin-Tie2 Signaling

Retraction: Endothelial cell‐specific deficiency of the adenosine deaminase ADAR1 aggravates LPS‐induced lung injury in mice via an MDA5‐independent pathway

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