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  1. AU=Renzi Tiziana Ada
  2. AU="Bekers, Wouter"

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  1. Article ; Online: MiR-146b Mediates Endotoxin Tolerance in Human Phagocytes.

    Renzi, Tiziana Ada / Rubino, Marcello / Gornati, Laura / Garlanda, Cecilia / Locati, Massimo / Curtale, Graziella

    Mediators of inflammation

    2015  Volume 2015, Page(s) 145305

    Abstract: A proper regulation of the innate immune response is fundamental to keep the immune system in check and avoid a chronic status of inflammation. As they act as negative modulators of TLR signaling pathways, miRNAs have been recently involved in the ... ...

    Abstract A proper regulation of the innate immune response is fundamental to keep the immune system in check and avoid a chronic status of inflammation. As they act as negative modulators of TLR signaling pathways, miRNAs have been recently involved in the control of the inflammatory response. However, their role in the context of endotoxin tolerance is just beginning to be explored. We here show that miR-146b is upregulated in human monocytes tolerized by LPS, IL-10, or TGFβ priming and demonstrate that its transcription is driven by STAT3 and RUNX3, key factors downstream of IL-10 and TGFβ signaling. Our study also found that IFNγ, known to revert LPS tolerant state, inhibits miR-146b expression. Finally, we provide evidence that miR-146b levels have a profound effect on the tolerant state, thus candidating miR-146b as a molecular mediator of endotoxin tolerance.
    MeSH term(s) Cell Line ; Cells, Cultured ; Chromatin Immunoprecipitation ; Endotoxins/pharmacology ; Enzyme-Linked Immunosorbent Assay ; Humans ; Immunoprecipitation ; Interleukin-10/pharmacology ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Monocytes/drug effects ; Monocytes/metabolism ; Phagocytes/drug effects ; Phagocytes/metabolism ; Transforming Growth Factor beta/pharmacology
    Chemical Substances Endotoxins ; MIRN146 microRNA, human ; MicroRNAs ; Transforming Growth Factor beta ; Interleukin-10 (130068-27-8)
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1137605-3
    ISSN 1466-1861 ; 0962-9351
    ISSN (online) 1466-1861
    ISSN 0962-9351
    DOI 10.1155/2015/145305
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3575: 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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  2. Article ; Online: Negative regulation of Toll-like receptor 4 signaling by IL-10-dependent microRNA-146b.

    Curtale, Graziella / Mirolo, Massimiliano / Renzi, Tiziana Ada / Rossato, Marzia / Bazzoni, Flavia / Locati, Massimo

    Proceedings of the National Academy of Sciences of the United States of America

    2013  Volume 110, Issue 28, Page(s) 11499–11504

    Abstract: Toll-like receptors (TLRs) play key roles in detecting pathogens and initiating inflammatory responses that, subsequently, prime specific adaptive responses. Several mechanisms control TLR activity to avoid excessive inflammation and consequent ... ...

    Abstract Toll-like receptors (TLRs) play key roles in detecting pathogens and initiating inflammatory responses that, subsequently, prime specific adaptive responses. Several mechanisms control TLR activity to avoid excessive inflammation and consequent immunopathology, including the anti-inflammatory cytokine IL-10. Recently, several TLR-responsive microRNAs (miRs) have also been proposed as potential regulators of this signaling pathway, but their functional role during the inflammatory response still is incompletely understood. In this study, we report that, after LPS engagement, monocytes up-regulate miR-146b via an IL-10-mediated STAT3-dependent loop. We show evidence that miR-146b modulates the TLR4 signaling pathway by direct targeting of multiple elements, including the LPS receptor TLR4 and the key adaptor/signaling proteins myeloid differentiation primary response (MyD88), interleukin-1 receptor-associated kinase 1 (IRAK-1), and TNF receptor-associated factor 6 (TRAF6). Furthermore, we demonstrate that the enforced expression of miR-146b in human monocytes led to a significant reduction in the LPS-dependent production of several proinflammatory cytokines and chemokines, including IL-6, TNF-α, IL-8, CCL3, CCL2, CCL7, and CXCL10. Our results thus identify miR-146b as an IL-10-responsive miR with an anti-inflammatory activity based on multiple targeting of components of the TLR4 pathway in monocytes and candidate miR-146b as a molecular effector of the IL-10 anti-inflammatory activity.
    MeSH term(s) Cells, Cultured ; Cytokines/biosynthesis ; Humans ; Inflammation Mediators/metabolism ; Interleukin-10/physiology ; MicroRNAs/physiology ; Monocytes/metabolism ; Signal Transduction/genetics ; Toll-Like Receptor 4/metabolism
    Chemical Substances Cytokines ; Inflammation Mediators ; MIRN146 microRNA, human ; MicroRNAs ; TLR4 protein, human ; Toll-Like Receptor 4 ; Interleukin-10 (130068-27-8)
    Language English
    Publishing date 2013-06-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1219852110
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: 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)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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