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  1. Article ; Online: Inhibition of YTHDF1 by salvianolic acid overcomes gluten-induced intestinal inflammation.

    Olazagoitia-Garmendia, Ane / Rojas-Márquez, Henar / Romero, Maria Del Mar / Ruiz, Pamela / Agirre-Lizaso, Aloña / Chen, Yantao / Perugorria, Maria Jesus / Herrero, Laura / Serra, Dolors / Luo, Cheng / Bujanda, Luis / He, Chuan / Castellanos-Rubio, Ainara

    Gut

    2023  

    Language English
    Publishing date 2023-10-31
    Publishing country England
    Document type Letter
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gutjnl-2023-330459
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Cardiotrophin-1 is an anti-inflammatory cytokine and promotes IL-4-induced M2 macrophage polarization.

    Carneros, David / Santamaría, Eva M / Larequi, Eduardo / Vélez-Ortiz, Jose Miguel / Reboredo, Mercedes / Mancheño, Uxua / Perugorria, María Jesús / Navas, Plácido / Romero-Gómez, Manuel / Prieto, Jesús / Hervás-Stubbs, Sandra / Bustos, Matilde

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

    2019  Volume 33, Issue 6, Page(s) 7578–7587

    Abstract: Macrophages play a central role in tissue remodeling, repair, and resolution of inflammation. Macrophage polarization to M1 or M2 activation status may determine the progression or resolution of the inflammatory response. We have previously reported that ...

    Abstract Macrophages play a central role in tissue remodeling, repair, and resolution of inflammation. Macrophage polarization to M1 or M2 activation status may determine the progression or resolution of the inflammatory response. We have previously reported that cardiotrophin-1 (CT-1) displays both cytoprotective and metabolic activities. The role of CT-1 in inflammation remains poorly understood. Here, we employed recombinant CT-1 (rCT-1) and used
    MeSH term(s) Animals ; Cell Polarity ; Cytokines/physiology ; Inflammation/prevention & control ; Interleukin-4/physiology ; Interleukin-6/physiology ; Macrophages/cytology ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic
    Chemical Substances Cytokines ; IL6 protein, human ; Il4 protein, mouse ; Interleukin-6 ; Interleukin-4 (207137-56-2) ; cardiotrophin 1 (AJ7U77BR8I)
    Language English
    Publishing date 2019-03-20
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639186-2
    ISSN 1530-6860 ; 0892-6638
    ISSN (online) 1530-6860
    ISSN 0892-6638
    DOI 10.1096/fj.201801563R
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: TREM-2 defends the liver against hepatocellular carcinoma through multifactorial protective mechanisms.

    Esparza-Baquer, Aitor / Labiano, Ibone / Sharif, Omar / Agirre-Lizaso, Aloña / Oakley, Fiona / Rodrigues, Pedro M / Zhuravleva, Ekaterina / O'Rourke, Colm J / Hijona, Elizabeth / Jimenez-Agüero, Raul / Riaño, Ioana / Landa, Ana / La Casta, Adelaida / Zaki, Marco Y W / Munoz-Garrido, Patricia / Azkargorta, Mikel / Elortza, Felix / Vogel, Andrea / Schabbauer, Gernot /
    Aspichueta, Patricia / Andersen, Jesper B / Knapp, Sylvia / Mann, Derek A / Bujanda, Luis / Banales, Jesus Maria / Perugorria, Maria Jesus

    Gut

    2020  Volume 70, Issue 7, Page(s) 1345–1361

    Abstract: Objective: Hepatocellular carcinoma (HCC) is a prevalent and aggressive cancer usually arising on a background of chronic liver injury involving inflammatory and hepatic regenerative processes. The triggering receptor expressed on myeloid cells 2 (TREM- ... ...

    Abstract Objective: Hepatocellular carcinoma (HCC) is a prevalent and aggressive cancer usually arising on a background of chronic liver injury involving inflammatory and hepatic regenerative processes. The triggering receptor expressed on myeloid cells 2 (TREM-2) is predominantly expressed in hepatic non-parenchymal cells and inhibits Toll-like receptor signalling, protecting the liver from various hepatotoxic injuries, yet its role in liver cancer is poorly defined. Here, we investigated the impact of TREM-2 on liver regeneration and hepatocarcinogenesis.
    Design: TREM-2 expression was analysed in liver tissues of two independent cohorts of patients with HCC and compared with control liver samples. Experimental HCC and liver regeneration models in wild type and
    Results: TREM-2
    Conclusion: TREM-2 plays a protective role in hepatocarcinogenesis via different pleiotropic effects, suggesting that TREM-2 agonism should be investigated as it might beneficially impact HCC pathogenesis in a multifactorial manner.
    MeSH term(s) Adult ; Aged ; Animals ; Carcinogenesis/genetics ; Carcinoma, Hepatocellular/chemically induced ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Carcinoma, Hepatocellular/pathology ; Cell Line, Tumor ; Cell Proliferation ; Diethylnitrosamine ; Female ; Gain of Function Mutation ; Gene Expression ; Hepatic Stellate Cells/metabolism ; Hepatitis/metabolism ; Hepatocytes/pathology ; Hepatocytes/physiology ; Humans ; Liver/metabolism ; Liver Cirrhosis/metabolism ; Liver Neoplasms/chemically induced ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; Liver Neoplasms/pathology ; Liver Regeneration/genetics ; Liver Regeneration/physiology ; Macrophages/metabolism ; Male ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/metabolism ; Mice ; Mice, Knockout ; Middle Aged ; Oxidative Stress ; Protective Factors ; RNA/metabolism ; Reactive Oxygen Species/metabolism ; Receptors, Immunologic/genetics ; Receptors, Immunologic/metabolism ; Spheroids, Cellular ; Up-Regulation ; Wnt Proteins/metabolism ; Wnt Signaling Pathway ; Wnt3 Protein/metabolism
    Chemical Substances Membrane Glycoproteins ; Reactive Oxygen Species ; Receptors, Immunologic ; TREM2 protein, human ; Trem2 protein, mouse ; WNT3 protein, human ; WNT7A protein, human ; WNT8A protein, human ; Wnt Proteins ; Wnt3 Protein ; Diethylnitrosamine (3IQ78TTX1A) ; RNA (63231-63-0)
    Language English
    Publishing date 2020-09-09
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gutjnl-2019-319227
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Histone methyltransferase ASH1 orchestrates fibrogenic gene transcription during myofibroblast transdifferentiation.

    Perugorria, Maria Jesus / Wilson, Caroline L / Zeybel, Mujdat / Walsh, Meagan / Amin, Shilu / Robinson, Stuart / White, Steven A / Burt, Alastair D / Oakley, Fiona / Tsukamoto, Hidekazu / Mann, Derek A / Mann, Jelena

    Hepatology (Baltimore, Md.)

    2012  Volume 56, Issue 3, Page(s) 1129–1139

    Abstract: Unlabelled: Transdifferentiation of hepatic stellate cells (HSCs) to a myofibroblast-like phenotype is the pivotal event in liver fibrosis. The dramatic change in phenotype associated with transdifferentiation is underpinned by a global change in gene ... ...

    Abstract Unlabelled: Transdifferentiation of hepatic stellate cells (HSCs) to a myofibroblast-like phenotype is the pivotal event in liver fibrosis. The dramatic change in phenotype associated with transdifferentiation is underpinned by a global change in gene expression. Orchestrated changes in gene expression take place at the level of chromatin packaging which is regulated by enzymatic activity of epigenetic regulators that in turn affect histone modifications. Using expression profiling of epigenetic regulators in quiescent and activated primary HSCs we found a number of histone methyltransferases including MLL1, MLL5, Set1 and ASH1 to be highly up-regulated during transdifferentiation of HSCs. All of these histone methyltransferases regulate methylation of lysine 4 of histone H3, which is a signature of actively transcribed genes. We therefore postulated that one or more of these enzymes may be involved in positively influencing expression of profibrogenic genes.
    Conclusion: We find that ASH1 directly binds to the regulatory regions of alpha smooth muscle actin (αSMA), collagen I, tissue inhibitor of metalloproteinase-1 (TIMP1) and transforming growth factor beta1 (TGFβ1) in activated HSCs while depletion of ASH1 caused broad suppression of fibrogenic gene expression. We also discovered that MeCP2 positively regulates ASH1 expression and therefore identify ASH1 as a key transcriptional activator component of the MeCP2 epigenetic relay pathway that orchestrates coordinated induction of multiple profibrogenic genes.
    MeSH term(s) Animals ; Basic Helix-Loop-Helix Transcription Factors/physiology ; Cell Transdifferentiation/genetics ; Fibrosis/genetics ; Histone Methyltransferases ; Histone-Lysine N-Methyltransferase/physiology ; Humans ; Mice ; Myofibroblasts/cytology ; Transcription, Genetic
    Chemical Substances Ascl1 protein, mouse ; Basic Helix-Loop-Helix Transcription Factors ; Histone Methyltransferases (EC 2.1.1.-) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
    Language English
    Publishing date 2012-04-03
    Publishing country United States
    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 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.25754
    Database MEDical Literature Analysis and Retrieval System OnLINE

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