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  1. Article ; Online: Finding the TRAIL to escape granzyme B-mediated liver injury in PSC.

    Guicciardi, Maria Eugenia / Jalan-Sakrikar, Nidhi

    Hepatology (Baltimore, Md.)

    2024  

    Language English
    Publishing date 2024-03-19
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1097/HEP.0000000000000859
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1660: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  2. Article ; Online: Burning, but Not Dying: the Failure of Pyroptotic Cell Death in Hepatocytes.

    Guicciardi, Maria Eugenia / Gores, Gregory J

    Cellular and molecular gastroenterology and hepatology

    2021  Volume 13, Issue 3, Page(s) 974–976

    MeSH term(s) Hepatocytes/metabolism ; Inflammasomes/metabolism ; Pyroptosis
    Chemical Substances Inflammasomes
    Language English
    Publishing date 2021-12-29
    Publishing country United States
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2819778-1
    ISSN 2352-345X ; 2352-345X
    ISSN (online) 2352-345X
    ISSN 2352-345X
    DOI 10.1016/j.jcmgh.2021.12.006
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: The Metabolic Sensor Adenosine Monophosphate-Activated Protein Kinase Regulates Apoptosis in Nonalcoholic Steatohepatitis.

    Guicciardi, Maria Eugenia / Nakao, Yasuhiko / Gores, Gregory J

    Hepatology (Baltimore, Md.)

    2020  Volume 72, Issue 3, Page(s) 1139–1141

    MeSH term(s) AMP-Activated Protein Kinases ; Adenosine Monophosphate ; Apoptosis ; Caspase 6 ; Humans ; Non-alcoholic Fatty Liver Disease
    Chemical Substances Adenosine Monophosphate (415SHH325A) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Caspase 6 (EC 3.4.22.-)
    Language English
    Publishing date 2020-04-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.31294
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  4. Article ; Online: Paving the TRAIL to anti-fibrotic therapy.

    Guicciardi, Maria Eugenia / Gores, Gregory J

    Hepatology (Baltimore, Md.)

    2016  Volume 64, Issue 1, Page(s) 29–31

    Language English
    Publishing date 2016-07
    Publishing country United States
    Document type Editorial
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.28520
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1660: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) deletion in myeloid cells augments cholestatic liver injury.

    Krishnan, Anuradha / Ozturk, Nazli Begum / Cutshaw, Kaiyel A / Guicciardi, Maria Eugenia / Kitagataya, Takashi / Olson, Kirsta E / Pavelko, Kevin D / Sherman, William / Wixom, Alexander Q / Jalan-Sakrikar, Nidhi / Baez-Faria, Michelle / Gutierrez, Florencia / Gores, Gregory J

    Scientific reports

    2024  Volume 14, Issue 1, Page(s) 2145

    Abstract: Ductular reactive (DR) cells exacerbate cholestatic liver injury and fibrosis. Herein, we posit that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) emanates from recruited macrophages and restrains DR cell expansion, thereby limiting ... ...

    Abstract Ductular reactive (DR) cells exacerbate cholestatic liver injury and fibrosis. Herein, we posit that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) emanates from recruited macrophages and restrains DR cell expansion, thereby limiting cholestatic liver injury. Wild type (WT), Trail
    MeSH term(s) Animals ; Mice ; Apoptosis/genetics ; Cholestasis/metabolism ; Fibrosis ; Ligands ; Liver/metabolism ; Macrophages/metabolism ; Mice, Inbred C57BL ; Tumor Necrosis Factor-alpha/metabolism
    Chemical Substances Ligands ; Tumor Necrosis Factor-alpha ; Tnfsf10 protein, mouse
    Language English
    Publishing date 2024-01-25
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-024-52710-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: IL-17 Signaling in Primary Sclerosing Cholangitis Patient-Derived Organoids.

    Garcia Moreno, Ana Sofia / Guicciardi, Maria Eugenia / Wixom, Alexander Q / Jessen, Erik / Yang, Jingchun / Ilyas, Sumera I / Bianchi, Jackie K / Pinto E Vairo, Filippo / Lazaridis, Konstantinos N / Gores, Gregory J

    Research square

    2023  

    Abstract: The pathogenesis of primary sclerosing cholangitis (PSC) is unclear, although studies implicate IL-17A as an inflammatory mediator in this disease. However, a direct assessment of IL-17 signaling in PSC cholangiocytes is lacking. In this study we aimed ... ...

    Abstract The pathogenesis of primary sclerosing cholangitis (PSC) is unclear, although studies implicate IL-17A as an inflammatory mediator in this disease. However, a direct assessment of IL-17 signaling in PSC cholangiocytes is lacking. In this study we aimed to investigate the response of PSC extrahepatic cholangiocyte organoids (ECO) to IL-17A stimulation. Cholangiocytes obtained from PSC and non-PSC patients by endoscopic retrograde cholangiography (ERC) were cultured as ECO. The ECO were treated with vehicle or IL-17A and assessed by transcriptomics, secretome analysis, and genome sequencing (GS). Unsupervised clustering of all integrated scRNA-seq data identified 8 cholangiocyte clusters which did not differ between PSC and non-PSC ECO. However, PSC ECO cells demonstrated a robust response to IL-17 treatment, noted by an increased number of differentially expressed genes (DEG) by transcriptomics, and more abundant chemokine and cytokine expression and secretion. After rigorous filtering, GS identified candidate somatic variants shared among PSC ECO from unrelated individuals. However, no candidate rare variants in genes regulating the IL-17 pathway were identified, but rare variants regulating the MAPK signaling pathway were present in all PSC ECO. In conclusion, PSC and non-PSC patient derived ECO respond differently to IL-17 stimulation implicating this pathway in the pathogenesis of PSC.
    Language English
    Publishing date 2023-10-16
    Publishing country United States
    Document type Preprint
    DOI 10.21203/rs.3.rs-3406046/v1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Proapoptotic signaling induced by deletion of receptor-interacting kinase 1 and TNF receptor-associated factor 2 results in liver carcinogenesis.

    Hirsova, Petra / Guicciardi, Maria Eugenia / Gores, Gregory J

    Hepatology (Baltimore, Md.)

    2017  Volume 66, Issue 3, Page(s) 983–985

    MeSH term(s) Apoptosis/drug effects ; Carcinogenesis ; Humans ; Liver ; NF-kappa B ; Signal Transduction/drug effects ; TNF Receptor-Associated Factor 2 ; Tumor Necrosis Factor-alpha
    Chemical Substances NF-kappa B ; TNF Receptor-Associated Factor 2 ; Tumor Necrosis Factor-alpha
    Language English
    Publishing date 2017-07-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.29272
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1660: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  8. Article ; Online: Complete lysosomal disruption: a route to necrosis, not to the inflammasome.

    Guicciardi, Maria Eugenia / Gores, Gregory J

    Cell cycle (Georgetown, Tex.)

    2013  Volume 12, Issue 13, Page(s) 1995

    MeSH term(s) Animals ; Carrier Proteins/metabolism ; Lysosomes/metabolism ; Necrosis/metabolism
    Chemical Substances Carrier Proteins
    Language English
    Publishing date 2013-06-11
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.4161/cc.25317
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5881: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  9. Article ; Online: The Spectrum of Reactive Cholangiocytes in Primary Sclerosing Cholangitis.

    Guicciardi, Maria Eugenia / Trussoni, Christy E / LaRusso, Nicholas F / Gores, Gregory J

    Hepatology (Baltimore, Md.)

    2019  Volume 71, Issue 2, Page(s) 741–748

    Abstract: Cholangiocytes are the target of a group of chronic liver diseases termed the "cholangiopathies," in which cholangiocytes react to exogenous and endogenous insults, leading to disease initiation and progression. In primary sclerosing cholangitis (PSC), ... ...

    Abstract Cholangiocytes are the target of a group of chronic liver diseases termed the "cholangiopathies," in which cholangiocytes react to exogenous and endogenous insults, leading to disease initiation and progression. In primary sclerosing cholangitis (PSC), the focus of this review, the cholangiocyte response to genetic or environmental insults can lead to a heterogeneous response; that is, a subpopulation acquires a ductular reactive and proliferative phenotype, while another subpopulation undergoes senescence and growth arrest. Both ductular reactive cholangiocytes and senescent cholangiocytes can modify the periductal microenvironment through their ability to secrete various cytokines, chemokines, and growth factors, initiating and perpetuating inflammatory and profibrotic responses. This review discusses the similarities and differences, the interrelationships, and the potential pathogenic roles of these reactive proliferative and senescent cholangiocyte subpopulations in PSC.
    MeSH term(s) Bile Ducts/cytology ; Cell Proliferation ; Cholangitis, Sclerosing/pathology ; Epithelial Cells/physiology ; Humans
    Language English
    Publishing date 2019-12-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.31067
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  10. Article ; Online: Unshackling caspase-7 for cancer therapy.

    Guicciardi, Maria Eugenia / Gores, Gregory J

    The Journal of clinical investigation

    2013  Volume 123, Issue 9, Page(s) 3706–3708

    Abstract: Numerous solid tumors and hematologic malignancies acquire resistance to apoptosis-inducing chemotherapeutic drugs by downregulating the key effector caspase-3. These cells rely on caspase-7 to execute the apoptotic program, yet binding with XIAP ... ...

    Abstract Numerous solid tumors and hematologic malignancies acquire resistance to apoptosis-inducing chemotherapeutic drugs by downregulating the key effector caspase-3. These cells rely on caspase-7 to execute the apoptotic program, yet binding with XIAP constitutively inhibits active caspase-7 (p19/p12-CASP7). In this issue, Lin et al. describe how a newly synthesized drug is able to disrupt the XIAP:p19/p12-CASP7 complex and induce apoptosis in caspase-3-deficient cancer cells in vitro and in vivo. As this compound appears to exhibit minimal toxicity on normal tissues, it may represent a promising therapeutic agent to help treat caspase-3-deficient tumors.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Caspase 3/deficiency ; Caspase 7/metabolism ; Drug Resistance, Neoplasm ; Female ; Humans ; Lysine/analogs & derivatives ; Lysine/pharmacology ; X-Linked Inhibitor of Apoptosis Protein/metabolism
    Chemical Substances Antineoplastic Agents ; X-Linked Inhibitor of Apoptosis Protein ; XIAP protein, human ; CASP3 protein, human (EC 3.4.22.-) ; CASP7 protein, human (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-) ; Caspase 7 (EC 3.4.22.-) ; Lysine (K3Z4F929H6)
    Language English
    Publishing date 2013-08-27
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI71440
    Database MEDical Literature Analysis and Retrieval System OnLINE

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