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  1. Article ; Online: IGFBP7- When Endothelial gCap-ing Goes Wrong in Acute Lung Injury.

    Surolia, Ranu / Zmijewski, Jaroslaw W

    American journal of respiratory cell and molecular biology

    2024  

    Language English
    Publishing date 2024-04-16
    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.2024-0146ED
    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:
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  2. Article ; Online: Autophagy in Idiopathic Pulmonary Fibrosis: Predisposition of the Aging Lung to Fibrosis?

    Zmijewski, Jaroslaw W / Thannickal, Victor J

    American journal of respiratory cell and molecular biology

    2023  Volume 68, Issue 1, Page(s) 3–4

    MeSH term(s) Humans ; Idiopathic Pulmonary Fibrosis/genetics ; Lung ; Aging ; Autophagy ; Ubiquitin-Specific Proteases
    Chemical Substances USP13 protein, human (EC 3.4.19.12) ; Ubiquitin-Specific Proteases (EC 3.4.19.12)
    Language English
    Publishing date 2023-02-10
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2022-0379ED
    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)
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  3. Article ; Online: Human Leukocyte Antigen-DR Deficiency and Immunosuppression-Related End-Organ Failure in SARS-CoV2 Infection.

    Zmijewski, Jaroslaw W / Pittet, Jean-Francois

    Anesthesia and analgesia

    2020  Volume 131, Issue 4, Page(s) 989–992

    MeSH term(s) Betacoronavirus ; COVID-19 ; Coronavirus Infections ; Critical Illness ; HLA Antigens ; Humans ; Pandemics ; Pneumonia, Viral ; SARS-CoV-2
    Chemical Substances HLA Antigens
    Keywords covid19
    Language English
    Publishing date 2020-12-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 80032-6
    ISSN 1526-7598 ; 0003-2999
    ISSN (online) 1526-7598
    ISSN 0003-2999
    DOI 10.1213/ANE.0000000000005140
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uk I Zs.78: Show issues Location:
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    Zs.MO 149: Show issues

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  4. Article ; Online: AMPK activation improves recovery from pneumonia-induced lung injury via reduction of er-stress and apoptosis in alveolar epithelial cells.

    Becker, Eugene / Husain, Maroof / Bone, Nathaniel / Smith, Samuel / Morris, Peter / Zmijewski, Jaroslaw W

    Respiratory research

    2023  Volume 24, Issue 1, Page(s) 185

    Abstract: Background: Bacterial pneumonia and related lung injury are among the most frequent causes of mortality in intensive care units, but also inflict serious and prolonged respiratory complications among survivors. Given that endoplasmic reticulum (ER) ... ...

    Abstract Background: Bacterial pneumonia and related lung injury are among the most frequent causes of mortality in intensive care units, but also inflict serious and prolonged respiratory complications among survivors. Given that endoplasmic reticulum (ER) stress is a hallmark of sepsis-related alveolar epithelial cell (AEC) dysfunction, we tested if AMP-activated protein kinase (AMPK) affects recovery from ER stress and apoptosis of AECs during post-bacterial infection.
    Methods: In a murine model of lung injury by P. aeruginosa non-lethal infection, therapeutic interventions included AMPK activator metformin or GSK-3β inhibitor Tideglusib for 96 h. Recovery from AEC injury was evidenced by accumulation of soluble T-1α (AEC Type 1 marker) in BAL fluids along with fluorescence analysis of ER-stress (CHOP) and apoptosis (TUNEL) in lung sections. AMPK phosphorylation status and mediators of ER stress were determined via Immunoblot analysis from lung homogenates. Macrophage-dependent clearance of apoptotic cells was determined using flow cytometry assay.
    Results: P. aeruginosa-induced lung injury resulted in accumulation of neutrophils and cellular debris in the alveolar space along with persistent (96 h) ER-stress and apoptosis of AECs. While lung infection triggered AMPK inactivation (de-phosphorylation of Thr172-AMPK), metformin and Tideglusib promptly restored the AMPK activation status. In post infected mice, AMPK activation reduced indices of lung injury, ER stress and related apoptosis of AECs, as early as 24 h post administration of AMPK activators. In addition, we demonstrate that the extent of apoptotic cell accumulation is also dependent on AMPK-mediated clearance of apoptotic cells by macrophages.
    Conclusions: Our study provides important insights into AMPK function in the preservation of AEC viability after bacterial infection, in particular due reduction of ER-stress and apoptosis, thereby promoting effective recovery from lung injury after pneumonia.
    MeSH term(s) Animals ; Mice ; Alveolar Epithelial Cells ; AMP-Activated Protein Kinases ; Glycogen Synthase Kinase 3 beta ; Lung Injury/drug therapy ; Apoptosis
    Chemical Substances tideglusib (Q747Y6TT42) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1)
    Language English
    Publishing date 2023-07-12
    Publishing country England
    Document type Journal Article
    ZDB-ID 2041675-1
    ISSN 1465-993X ; 1465-993X
    ISSN (online) 1465-993X
    ISSN 1465-993X
    DOI 10.1186/s12931-023-02483-6
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Human Leukocyte Antigen-DR Deficiency and Immunosuppression-Related End-Organ Failure in SARS-CoV2 Infection

    Zmijewski, Jaroslaw W. / Pittet, Jean-Francois

    Anesthesia & Analgesia

    2020  Volume 131, Issue 4, Page(s) 989–992

    Keywords Anesthesiology and Pain Medicine ; covid19
    Language English
    Publisher Ovid Technologies (Wolters Kluwer Health)
    Publishing country us
    Document type Article ; Online
    ZDB-ID 80032-6
    ISSN 1526-7598 ; 0003-2999
    ISSN (online) 1526-7598
    ISSN 0003-2999
    DOI 10.1213/ane.0000000000005140
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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    Zs.MO 149: Show issues

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  7. Article ; Online: PAI-1 Regulation of p53 Expression and Senescence in Type II Alveolar Epithelial Cells.

    Rana, Tapasi / Jiang, Chunsun / Banerjee, Sami / Yi, Nengjun / Zmijewski, Jaroslaw W / Liu, Gang / Liu, Rui-Ming

    Cells

    2023  Volume 12, Issue 15

    Abstract: Cellular senescence contributes importantly to aging and aging-related diseases, including idiopathic pulmonary fibrosis (IPF). Alveolar epithelial type II (ATII) cells are progenitors of alveolar epithelium, and ATII cell senescence is evident in IPF. ... ...

    Abstract Cellular senescence contributes importantly to aging and aging-related diseases, including idiopathic pulmonary fibrosis (IPF). Alveolar epithelial type II (ATII) cells are progenitors of alveolar epithelium, and ATII cell senescence is evident in IPF. Previous studies from this lab have shown that increased expression of plasminogen activator inhibitor 1 (PAI-1), a serine protease inhibitor, promotes ATII cell senescence through inducing p53, a master cell cycle repressor, and activating p53-p21-pRb cell cycle repression pathway. In this study, we further show that PAI-1 binds to proteasome components and inhibits proteasome activity and p53 degradation in human lung epithelial A549 cells and primary mouse ATII cells. This is associated with a senescence phenotype of these cells, manifested as increased p53 and p21 expression, decreased phosphorylated retinoblastoma protein (pRb), and increased senescence-associated beta-galactose (SA-β-gal) activity. Moreover, we find that, although overexpression of wild-type PAI-1 (wtPAI-1) or a secretion-deficient, mature form of PAI-1 (sdPAI-1) alone induces ATII cell senescence (increases SA-β-gal activity), only wtPAI-1 induces p53, suggesting that the premature form of PAI-1 is required for the interaction with the proteasome. In summary, our data indicate that PAI-1 can bind to proteasome components and thus inhibit proteasome activity and p53 degradation in ATII cells. As p53 is a master cell cycle repressor and PAI-1 expression is increased in many senescent cells, the results from this study will have a significant impact not only on ATII cell senescence/lung fibrosis but also on the senescence of other types of cells in different diseases.
    MeSH term(s) Animals ; Humans ; Mice ; Alveolar Epithelial Cells/metabolism ; Idiopathic Pulmonary Fibrosis/metabolism ; Plasminogen Activator Inhibitor 1/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Plasminogen Activator Inhibitor 1 ; Proteasome Endopeptidase Complex (EC 3.4.25.1) ; Tumor Suppressor Protein p53 ; SERPINE1 protein, human ; TP53 protein, human ; Trp53 protein, mouse
    Language English
    Publishing date 2023-08-05
    Publishing country Switzerland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12152008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Mitochondrial Dysfunction and Immune Cell Metabolism in Sepsis.

    Park, Dae Won / Zmijewski, Jaroslaw W

    Infection & chemotherapy

    2017  Volume 49, Issue 1, Page(s) 10–21

    Abstract: Sepsis is a life threatening condition mediated by systemic infection, but also triggered by hemorrhage and trauma. These are significant causes of organ injury implicated in morbidity and mortality, as well as post-sepsis complications associated with ... ...

    Abstract Sepsis is a life threatening condition mediated by systemic infection, but also triggered by hemorrhage and trauma. These are significant causes of organ injury implicated in morbidity and mortality, as well as post-sepsis complications associated with dysfunction of innate and adaptive immunity. The role of cellular bioenergetics and loss of metabolic plasticity of immune cells is increasingly emerging in the pathogenesis of sepsis. This review describes mitochondrial biology and metabolic alterations of immune cells due to sepsis, as well as indicates plausible therapeutic opportunities.
    Language English
    Publishing date 2017-04-05
    Publishing country Korea (South)
    Document type Journal Article ; Review
    ZDB-ID 2573798-3
    ISSN 2093-2340
    ISSN 2093-2340
    DOI 10.3947/ic.2017.49.1.10
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: NOX2 decoy peptides disrupt trauma-mediated neutrophil immunosuppression and protect against lethal peritonitis.

    Husain, Maroof / Becker, Eugene J / Bone, Nathaniel B / Schmitt, Amy / Pittet, Jean-Francois / Zmijewski, Jaroslaw W

    Redox biology

    2020  Volume 36, Page(s) 101651

    Abstract: Trauma and sepsis are frequent causes of immunosuppression and risk of secondary bacterial infections and mortality among critically ill patients. Reduced activity of neutrophil NADPH oxidase 2 (NOX2) and impaired bacterial killing are among the major ... ...

    Abstract Trauma and sepsis are frequent causes of immunosuppression and risk of secondary bacterial infections and mortality among critically ill patients. Reduced activity of neutrophil NADPH oxidase 2 (NOX2) and impaired bacterial killing are among the major indices of immunosuppression. We hypothesize that NOX2-decoy peptides disrupt the inhibition of neutrophil NOX2 by plasma of patients with severe trauma and immunosuppression, thereby preserving the neutrophil respiratory burst that is a central antimicrobial mechanism. We demonstrate that plasma from trauma/hemorrhage (T/H) patients, but not healthy donors (HD), significantly reduced the activity of neutrophil NOX2 and impaired bacterial killing. The inhibitory action of plasma was associated with an increase in bacterial infections among trauma survivors. High Mobility Group Box 1 (HMGB1) is a mediator of lethality in trauma and sepsis and our mechanistic studies revealed that disulfide and oxidized forms of HMGB1 bind to the gp91
    MeSH term(s) Animals ; Humans ; Immunosuppression ; Mice ; NADPH Oxidase 2/genetics ; NADPH Oxidases/genetics ; Neutrophils ; Peptides ; Peritonitis
    Chemical Substances Peptides ; NADPH Oxidase 2 (EC 1.6.3.-) ; NADPH Oxidases (EC 1.6.3.-)
    Language English
    Publishing date 2020-07-30
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2020.101651
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Bioenergetic maladaptation and release of HMGB1 in calcineurin inhibitor-mediated nephrotoxicity.

    Zmijewska, Anna A / Zmijewski, Jaroslaw W / Becker, Eugene J / Benavides, Gloria A / Darley-Usmar, Victor / Mannon, Roslyn B

    American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons

    2021  Volume 21, Issue 9, Page(s) 2964–2977

    Abstract: Calcineurin inhibitors (CNIs) are potent immunosuppressive agents, universally used following solid organ transplantation to prevent rejection. Although effective, the long-term use of CNIs is associated with nephrotoxicity. The etiology of this adverse ... ...

    Abstract Calcineurin inhibitors (CNIs) are potent immunosuppressive agents, universally used following solid organ transplantation to prevent rejection. Although effective, the long-term use of CNIs is associated with nephrotoxicity. The etiology of this adverse effect is complex, and effective therapeutic interventions remain to be determined. Using a combination of in vitro techniques and a mouse model of CNI-mediated nephrotoxicity, we found that the CNIs, cyclosporine A (CsA), and tacrolimus (TAC) share a similar mechanism of tubular epithelial kidney cell injury, including mitochondrial dysfunction and release of High-Mobility Group Box I (HMGB1). CNIs promote bioenergetic reprogramming due to mitochondrial dysfunction and a shift toward glycolytic metabolism. These events were accompanied by diminished cell-to-cell adhesion, loss of the epithelial cell phenotype, and release of HMGB1. Notably, Erk1/2 inhibitors effectively diminished HMGB1 release, and similar inhibitor was observed on inclusion of pan-caspase inhibitor zVAD-FMK. In vivo, while CNIs activate tissue proremodeling signaling pathways, MAPK/Erk1/2 inhibitor prevented nephrotoxicity, including diminished HMGB1 release from kidney epithelial cells and accumulation in urine. In summary, HMGB1 is an early indicator and marker of progressive nephrotoxicity induced by CNIs. We suggest that proremodeling signaling pathway and loss of mitochondrial redox/bioenergetics homeostasis are crucial therapeutic targets to ameliorate CNI-mediated nephrotoxicity.
    MeSH term(s) Animals ; Calcineurin Inhibitors/adverse effects ; Cyclosporine/adverse effects ; Energy Metabolism ; HMGB1 Protein ; Immunosuppressive Agents/adverse effects ; Mice ; Tacrolimus/toxicity
    Chemical Substances Calcineurin Inhibitors ; HMGB1 Protein ; Immunosuppressive Agents ; Cyclosporine (83HN0GTJ6D) ; Tacrolimus (WM0HAQ4WNM)
    Language English
    Publishing date 2021-04-02
    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 2060594-8
    ISSN 1600-6143 ; 1600-6135
    ISSN (online) 1600-6143
    ISSN 1600-6135
    DOI 10.1111/ajt.16561
    Database MEDical Literature Analysis and Retrieval System OnLINE

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