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  1. Article: Pulmonary Endothelial Cell Apoptosis in Emphysema and Acute Lung Injury.

    Chambers, Eboni / Rounds, Sharon / Lu, Qing

    Advances in anatomy, embryology, and cell biology

    2018  Volume 228, Page(s) 63–86

    Abstract: Apoptosis plays an essential role in homeostasis and pathogenesis of a variety of human diseases. Endothelial cells are exposed to various environmental and internal stress and endothelial apoptosis is a pathophysiological consequence of these stimuli. ... ...

    Abstract Apoptosis plays an essential role in homeostasis and pathogenesis of a variety of human diseases. Endothelial cells are exposed to various environmental and internal stress and endothelial apoptosis is a pathophysiological consequence of these stimuli. Pulmonary endothelial cell apoptosis initiates or contributes to progression of a number of lung diseases. This chapter will focus on the current understanding of the role of pulmonary endothelial cell apoptosis in the development of emphysema and acute lung injury (ALI) and the factors controlling pulmonary endothelial life and death.
    MeSH term(s) Acute Lung Injury/pathology ; Animals ; Apoptosis ; Autophagy ; Disease Models, Animal ; Endothelial Cells/pathology ; Humans ; Lung/cytology ; Lung/pathology ; Pulmonary Emphysema/pathology ; Respiratory Distress Syndrome, Adult/pathology ; Respiratory Mucosa/cytology ; Respiratory Mucosa/pathology
    Language English
    Publishing date 2018-01-08
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ISSN 0301-5556
    ISSN 0301-5556
    DOI 10.1007/978-3-319-68483-3_4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: NLRP3 inflammasome activation in cigarette smoke priming for Pseudomonas aeruginosa-induced acute lung injury.

    White, Alexis / Wang, Zhengke / Wang, Xing / King, Michelle / Guo, Cynthia / Mantsounga, Chris / Ayala, Alfred / Morrison, Alan R / Choudhary, Gaurav / Sellke, Frank / Chambers, Eboni / Ware, Lorraine B / Rounds, Sharon / Lu, Qing

    Redox biology

    2022  Volume 57, Page(s) 102467

    Abstract: It is increasingly recognized that cigarette smoke (CS) exposure increases the incidence and severity of acute respiratory distress syndrome (ARDS) in critical ill humans and animals. However, the mechanism(s) is not well understood. This study aims to ... ...

    Abstract It is increasingly recognized that cigarette smoke (CS) exposure increases the incidence and severity of acute respiratory distress syndrome (ARDS) in critical ill humans and animals. However, the mechanism(s) is not well understood. This study aims to investigate mechanism underlying the priming effect of CS on Pseudomonas aeruginosa-triggered acute lung injury, by using pre-clinic animal models and genetically modified mice. We demonstrated that CS impaired P. aeruginosa-induced mitophagy flux, promoted p62 accumulation, and exacerbated P. aeruginosa-triggered mitochondrial damage and NLRP3 inflammasome activation in alveolar macrophages; an effect associated with increased acute lung injury and mortality. Pharmacological inhibition of caspase-1, a component of inflammasome, attenuated CS primed P. aeruginosa-triggered acute lung injury and improved animal survival. Global or myeloid-specific knockout of IL-1β, a downstream component of inflammasome activation, also attenuated CS primed P. aeruginosa-triggered acute lung injury. Our results suggest that NLRP3 inflammasome activation is an important mechanism for CS primed P. aeruginosa-triggered acute lung injury. (total words: 155).
    MeSH term(s) Humans ; Mice ; Animals ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; Pseudomonas aeruginosa ; Cigarette Smoking ; Acute Lung Injury/chemically induced ; Mice, Inbred C57BL
    Chemical Substances Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse
    Language English
    Publishing date 2022-09-15
    Publishing country Netherlands
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2022.102467
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Cigarette Smoke Disrupted Lung Endothelial Barrier Integrity and Increased Susceptibility to Acute Lung Injury via Histone Deacetylase 6.

    Borgas, Diana / Chambers, Eboni / Newton, Julie / Ko, Junsuk / Rivera, Stephanie / Rounds, Sharon / Lu, Qing

    American journal of respiratory cell and molecular biology

    2016  Volume 54, Issue 5, Page(s) 683–696

    Abstract: Epidemiologic evidence indicates that cigarette smoke (CS) is associated with the development of acute lung injury (ALI). We have previously shown that brief CS exposure exacerbates lipopolysaccharide (LPS)-induced ALI in vivo and endothelial barrier ... ...

    Abstract Epidemiologic evidence indicates that cigarette smoke (CS) is associated with the development of acute lung injury (ALI). We have previously shown that brief CS exposure exacerbates lipopolysaccharide (LPS)-induced ALI in vivo and endothelial barrier dysfunction in vitro. In this study, we found that CS also exacerbated Pseudomonas-induced ALI in mice. We demonstrated that lung microvascular endothelial cells (ECs) isolated from mice exposed to CS had a greater permeability or incomplete recovery after challenges by LPS and thrombin. Histone deacetylase (HDAC) 6 deacetylates proteins essential for maintenance of endothelial barrier function. We found that HDAC6 phosphorylation at serine-22 was increased in lung tissues of mice exposed to CS and in lung ECs exposed to cigarette smoke extract (CSE). Inhibition of HDAC6 attenuated CSE-induced increases in EC permeability and CS priming of ALI. Similar barrier protection was provided by the microtubule stabilizer taxol, which preserved α-tubulin acetylation. CSE decreased α-tubulin acetylation and caused microtubule depolymerization. In coordination with increased HDAC6 phosphorylation, CSE inhibited Akt and activated glycogen synthase kinase (GSK)-3β; these effects were ameliorated by the antioxidant N-acetyl cysteine. Our results suggest that CS increases lung EC permeability, thereby enhancing susceptibility to ALI, likely through oxidative stress-induced Akt inactivation and subsequent GSK-3β activation. Activated GSK-3β may activate HDAC6 via phosphorylation of serine-22, leading to α-tubulin deacetylation and microtubule disassembly. Inhibition of HDAC6 may be a novel therapeutic option for ALI in cigarette smokers.
    MeSH term(s) Acute Lung Injury/enzymology ; Acute Lung Injury/microbiology ; Acute Lung Injury/pathology ; Animals ; Cattle ; Cell Membrane Permeability/drug effects ; Disease Susceptibility ; Endothelial Cells/drug effects ; Endothelial Cells/enzymology ; Endothelial Cells/microbiology ; Endothelial Cells/pathology ; Endothelium, Vascular/enzymology ; Endothelium, Vascular/pathology ; Glycogen Synthase Kinase 3 beta/metabolism ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylases/metabolism ; Humans ; Lipopolysaccharides/pharmacology ; Lung/pathology ; Male ; Mice, Inbred C57BL ; Microvessels/pathology ; Oxidative Stress/drug effects ; Phosphorylation/drug effects ; Proto-Oncogene Proteins c-akt/metabolism ; Pseudomonas aeruginosa/drug effects ; Pseudomonas aeruginosa/physiology ; Smoking/adverse effects
    Chemical Substances Histone Deacetylase Inhibitors ; Lipopolysaccharides ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Histone Deacetylases (EC 3.5.1.98)
    Language English
    Publishing date 2016-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2015-0149OC
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2851: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Blockade of equilibrative nucleoside transporter 1/2 protects against Pseudomonas aeruginosa-induced acute lung injury and NLRP3 inflammasome activation.

    Chambers, Eboni D / White, Alexis / Vang, Alexander / Wang, Zhengke / Ayala, Alfred / Weng, Tingting / Blackburn, Michael / Choudhary, Gaurav / Rounds, Sharon / Lu, Qing

    FASEB journal : official publication of the Federation of American Societies for Experimental Biology

    2019  Volume 34, Issue 1, Page(s) 1516–1531

    Abstract: Pseudomonas aeruginosa infections are increasingly multidrug resistant and cause healthcare-associated pneumonia, a major risk factor for acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Adenosine is a signaling nucleoside with ... ...

    Abstract Pseudomonas aeruginosa infections are increasingly multidrug resistant and cause healthcare-associated pneumonia, a major risk factor for acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Adenosine is a signaling nucleoside with potential opposing effects; adenosine can either protect against acute lung injury via adenosine receptors or cause lung injury via adenosine receptors or equilibrative nucleoside transporter (ENT)-dependent intracellular adenosine uptake. We hypothesized that blockade of intracellular adenosine uptake by inhibition of ENT1/2 would increase adenosine receptor signaling and protect against P. aeruginosa-induced acute lung injury. We observed that P. aeruginosa (strain: PA103) infection induced acute lung injury in C57BL/6 mice in a dose- and time-dependent manner. Using ENT1/2 pharmacological inhibitor, nitrobenzylthioinosine (NBTI), and ENT1-null mice, we demonstrated that ENT blockade elevated lung adenosine levels and significantly attenuated P. aeruginosa-induced acute lung injury, as assessed by lung wet-to-dry weight ratio, BAL protein levels, BAL inflammatory cell counts, pro-inflammatory cytokines, and pulmonary function (total lung volume, static lung compliance, tissue damping, and tissue elastance). Using both agonists and antagonists directed against adenosine receptors A
    MeSH term(s) Acute Lung Injury/drug therapy ; Acute Lung Injury/metabolism ; Acute Lung Injury/microbiology ; Acute Lung Injury/pathology ; Animals ; Equilibrative Nucleoside Transporter 1/antagonists & inhibitors ; Equilibrative Nucleoside Transporter 1/metabolism ; Equilibrative-Nucleoside Transporter 2/antagonists & inhibitors ; Equilibrative-Nucleoside Transporter 2/metabolism ; Inflammasomes/metabolism ; Male ; Mice ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Pseudomonas Infections/drug therapy ; Pseudomonas Infections/metabolism ; Pseudomonas Infections/pathology ; Pseudomonas aeruginosa/metabolism ; Thioinosine/analogs & derivatives ; Thioinosine/pharmacology
    Chemical Substances Equilibrative Nucleoside Transporter 1 ; Equilibrative-Nucleoside Transporter 2 ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; SLC29A1 protein, mouse ; Slc29a2 protein, mouse ; Thioinosine (46S541971T) ; 4-nitrobenzylthioinosine (GV1L2DZM2Z)
    Language English
    Publishing date 2019-12-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.201902286R
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2266: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 296: Show issues

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  5. Article ; Online: Alda-1 Protects Against Acrolein-induced Acute Lung Injury and Endothelial Barrier Dysfunction.

    Lu, Qing / Mundy, Miles / Chambers, Eboni / Lange, Thilo / Newton, Julie / Borgas, Diana / Yao, Hongwei / Choudhary, Gaurav / Basak, Rajshekhar / Oldham, Mahogany / Rounds, Sharon

    American journal of respiratory cell and molecular biology

    2017  

    Abstract: Inhalation of acrolein, a highly reactive aldehyde, causes lung edema. The underlying mechanism is poorly understood and there is no effective treatment. In this study, we demonstrated that acrolein not only dose-dependently induced lung edema, but also ... ...

    Abstract Inhalation of acrolein, a highly reactive aldehyde, causes lung edema. The underlying mechanism is poorly understood and there is no effective treatment. In this study, we demonstrated that acrolein not only dose-dependently induced lung edema, but also promoted lipopolysaccharide (LPS)-induced acute lung injury (ALI). Importantly, acrolein-induced lung injury were prevented and rescued by Alda-1, an activator of mitochondrial aldehyde dehydrogenase (ALDH) 2. Acrolein also dose-dependently increased monolayer permeability, disrupted adherens junctions and focal adhesion complexes, and caused intercellular gap formation in primary cultured lung microvascular endothelial cells (LMVEC); effects that were attenuated by Alda-1 and the antioxidant, N-acetylcysteine, but not by the NADPH inhibitor, apocynin. Furthermore, acrolein inhibited AMP-activated protein kinase (AMPK) and increased mitochondrial ROS levels in LMVEC; effects associated with impaired mitochondrial respiration. AMPK total protein levels were also reduced in lung tissue of mice and LMVEC exposed to acrolein. Activation of AMPK with AICAR blunted acrolein-induced increase in endothelial monolayer permeability, but not mitochondrial oxidative stress or inhibition of mitochondrial respiration. Our results suggest that acrolein-induced mitochondrial dysfunction may not contribute to endothelial barrier dysfunction. We speculate that detoxification of acrolein by Alda-1 and activation of AMPK may be novel approaches to prevent and treat acrolein-associated ALI, which may occur after smoke inhalation.
    Language English
    Publishing date 2017-08-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2016-0342OC
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2851: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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