LIVIVO - Das Suchportal für Lebenswissenschaften

switch to English language
Zurück zur letzten Suche Suchhistorie
Erweiterte Suche

Ihre letzten Suchen

  1. AU="Hizir, Zoheir"
  2. AU="Merrell, Allyson J"
  3. AU="Marie I. Samanovic"
  4. AU="Journeaux, Alexandre"
  5. AU="Cao, Mei Juan"
  6. AU="Wang, Hua-Yu"
  7. AU="Posner, Clara"
  8. AU="Gomes Da Silva, G"
  9. AU="Thoma, Tizia"
  10. AU="Liu, Huixing"
  11. AU="Mita-Mendoza, Neida K"
  12. AU="Anderson, Richard C E"
  13. AU="Garcia, Paula"
  14. AU="Soumya Nayak"

Suchergebnis

Treffer 1 - 5 von insgesamt 5

Suchoptionen

  1. Artikel ; Online: Valeur diagnostique des petits ARN dérivés des ARNY (ou RNY) dans les cardiopathies coronariennes.

    Hizir, Zoheir / Trabucchi, Michele / Repetto, Emanuela

    Medecine sciences : M/S

    2016  Band 32, Heft 3, Seite(n) 248–251

    Titelübersetzung Diagnostic value of YRNA-derived small RNAs for coronary artery disease.
    Mesh-Begriff(e) Autoantigens/physiology ; Biomarkers ; Coronary Artery Disease/diagnosis ; Coronary Artery Disease/genetics ; Humans ; MicroRNAs/isolation & purification ; MicroRNAs/physiology ; Predictive Value of Tests ; Prognosis ; RNA, Small Cytoplasmic/physiology ; Ribonucleoproteins/physiology
    Chemische Substanzen Autoantigens ; Biomarkers ; MicroRNAs ; RNA, Small Cytoplasmic ; RO60 protein, human ; Ribonucleoproteins
    Sprache Französisch
    Erscheinungsdatum 2016-03-23
    Erscheinungsland France
    Dokumenttyp News
    ZDB-ID 632733-3
    ISSN 1958-5381 ; 0767-0974
    ISSN (online) 1958-5381
    ISSN 0767-0974
    DOI 10.1051/medsci/20163203008
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Zs.B 2872: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  2. Artikel ; Online: RNY (YRNA)-derived small RNAs regulate cell death and inflammation in monocytes/macrophages.

    Hizir, Zoheir / Bottini, Silvia / Grandjean, Valerie / Trabucchi, Michele / Repetto, Emanuela

    Cell death & disease

    2017  Band 8, Heft 1, Seite(n) e2530

    Abstract: The recent discovery of new classes of small RNAs has opened unknown territories to explore new regulations of physiopathological events. We have recently demonstrated that RNY (or Y RNA)-derived small RNAs (referred to as s-RNYs) are an independent ... ...

    Abstract The recent discovery of new classes of small RNAs has opened unknown territories to explore new regulations of physiopathological events. We have recently demonstrated that RNY (or Y RNA)-derived small RNAs (referred to as s-RNYs) are an independent class of clinical biomarkers to detect coronary artery lesions and are associated with atherosclerosis burden. Here, we have studied the role of s-RNYs in human and mouse monocytes/macrophages and have shown that in lipid-laden monocytes/macrophages s-RNY expression is timely correlated to the activation of both NF-κB and caspase 3-dependent cell death pathways. Loss- or gain-of-function experiments demonstrated that s-RNYs activate caspase 3 and NF-κB signaling pathways ultimately promoting cell death and inflammatory responses. As, in atherosclerosis, Ro60-associated s-RNYs generated by apoptotic macrophages are released in the blood of patients, we have investigated the extracellular function of the s-RNY/Ro60 complex. Our data demonstrated that s-RNY/Ro60 complex induces caspase 3-dependent cell death and NF-κB-dependent inflammation, when added to the medium of cultured monocytes/macrophages. Finally, we have shown that s-RNY function is mediated by Toll-like receptor 7 (TLR7). Indeed using chloroquine, which disrupts signaling of endosome-localized TLRs 3, 7, 8 and 9 or the more specific TLR7/9 antagonist, the phosphorothioated oligonucleotide IRS954, we blocked the effect of either intracellular or extracellular s-RNYs. These results position s-RNYs as relevant novel functional molecules that impacts on macrophage physiopathology, indicating their potential role as mediators of inflammatory diseases, such as atherosclerosis.
    Mesh-Begriff(e) Animals ; Apoptosis/genetics ; Atherosclerosis/genetics ; Atherosclerosis/metabolism ; Atherosclerosis/pathology ; Autoantigens/genetics ; Autoantigens/metabolism ; Caspase 3/genetics ; Caspase 3/metabolism ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/pathology ; Macrophages/metabolism ; Macrophages/pathology ; Mice ; Monocytes/metabolism ; Monocytes/pathology ; RNA, Small Cytoplasmic/genetics ; RNA, Small Cytoplasmic/metabolism ; Ribonucleoproteins/genetics ; Ribonucleoproteins/metabolism ; Toll-Like Receptor 7/genetics
    Chemische Substanzen Autoantigens ; RNA, Small Cytoplasmic ; RO60 protein, human ; Ribonucleoproteins ; TLR7 protein, human ; Toll-Like Receptor 7 ; Caspase 3 (EC 3.4.22.-)
    Sprache Englisch
    Erscheinungsdatum 2017-01-05
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 2541626-1
    ISSN 2041-4889 ; 2041-4889
    ISSN (online) 2041-4889
    ISSN 2041-4889
    DOI 10.1038/cddis.2016.429
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

  3. Artikel ; Online: Control of APOBEC3B induction and cccDNA decay by NF-κB and miR-138-5p.

    Faure-Dupuy, Suzanne / Riedl, Tobias / Rolland, Maude / Hizir, Zoheir / Reisinger, Florian / Neuhaus, Katharina / Schuehle, Svenja / Remouchamps, Caroline / Gillet, Nicolas / Schönung, Maximilian / Stadler, Mira / Wettengel, Jochen / Barnault, Romain / Parent, Romain / Schuster, Linda Christina / Farhat, Rayan / Prokosch, Sandra / Leuchtenberger, Corinna / Öllinger, Rupert /
    Engleitner, Thomas / Rippe, Karsten / Rad, Roland / Unger, Kristian / Tscharahganeh, Darjus / Lipka, Daniel B / Protzer, Ulrike / Durantel, David / Lucifora, Julie / Dejardin, Emmanuel / Heikenwälder, Mathias

    JHEP reports : innovation in hepatology

    2021  Band 3, Heft 6, Seite(n) 100354

    Abstract: Background & aims: Immune-mediated induction of cytidine deaminase APOBEC3B (A3B) expression leads to HBV covalently closed circular DNA (cccDNA) decay. Here, we aimed to decipher the signalling pathway(s) and regulatory mechanism(s) involved in A3B ... ...

    Abstract Background & aims: Immune-mediated induction of cytidine deaminase APOBEC3B (A3B) expression leads to HBV covalently closed circular DNA (cccDNA) decay. Here, we aimed to decipher the signalling pathway(s) and regulatory mechanism(s) involved in A3B induction and related HBV control.
    Methods: Differentiated HepaRG cells (dHepaRG) knocked-down for NF-κB signalling components, transfected with siRNA or micro RNAs (miRNA), and primary human hepatocytes ± HBV or HBVΔX or HBV-RFP, were treated with lymphotoxin beta receptor (LTβR)-agonist (BS1). The biological outcomes were analysed by reverse transcriptase-qPCR, immunoblotting, luciferase activity, chromatin immune precipitation, electrophoretic mobility-shift assay, targeted-bisulfite-, miRNA-, RNA-, genome-sequencing, and mass-spectrometry.
    Results: We found that canonical and non-canonical NF-κB signalling pathways are mandatory for A3B induction and anti-HBV effects. The degree of immune-mediated A3B production is independent of A3B promoter demethylation but is controlled post-transcriptionally by the miRNA 138-5p expression (hsa-miR-138-5p), promoting A3B mRNA decay. Hsa-miR-138-5p over-expression reduced A3B levels and its antiviral effects. Of note, established infection inhibited BS1-induced A3B expression through epigenetic modulation of A3B promoter. Twelve days of treatment with a LTβR-specific agonist BS1 is sufficient to reduce the cccDNA pool by 80% without inducing significant damages to a subset of cancer-related host genes. Interestingly, the A3B-mediated effect on HBV is independent of the transcriptional activity of cccDNA as well as on rcDNA synthesis.
    Conclusions: Altogether, A3B represents the only described enzyme to target both transcriptionally active and inactive cccDNA. Thus, inhibiting hsa-miR-138-5p expression should be considered in the combinatorial design of new therapies against HBV, especially in the context of immune-mediated A3B induction.
    Lay summary: Immune-mediated induction of cytidine deaminase APOBEC3B is transcriptionally regulated by NF-κB signalling and post-transcriptionally downregulated by hsa-miR-138-5p expression, leading to cccDNA decay. Timely controlled APOBEC3B-mediated cccDNA decay occurs independently of cccDNA transcriptional activity and without damage to a subset of cancer-related genes. Thus, APOBEC3B-mediated cccDNA decay could offer an efficient therapeutic alternative to target hepatitis B virus chronic infection.
    Sprache Englisch
    Erscheinungsdatum 2021-08-25
    Erscheinungsland Netherlands
    Dokumenttyp Journal Article
    ISSN 2589-5559
    ISSN (online) 2589-5559
    DOI 10.1016/j.jhepr.2021.100354
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Zusatzmaterialien

    Kategorien

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  4. Artikel ; Online: RNY-derived small RNAs as a signature of coronary artery disease.

    Repetto, Emanuela / Lichtenstein, Laeticia / Hizir, Zoheir / Tekaya, Nedra / Benahmed, Mohamed / Ruidavets, Jean-Bernard / Zaragosi, Laure-Emmanuelle / Perret, Bertrand / Bouchareychas, Laura / Genoux, Annelise / Lotte, Romain / Ruimy, Raymond / Ferrières, Jean / Barbry, Pascal / Martinez, Laurent O / Trabucchi, Michele

    BMC medicine

    2015  Band 13, Seite(n) 259

    Abstract: Background: Data from next generation sequencing technologies uncovered the existence of many classes of small RNAs. Recent studies reported that small RNAs are released by cells and can be detected in the blood. In this report, we aimed to discover the ...

    Abstract Background: Data from next generation sequencing technologies uncovered the existence of many classes of small RNAs. Recent studies reported that small RNAs are released by cells and can be detected in the blood. In this report, we aimed to discover the occurrence of novel circulating small RNAs in coronary artery disease (CAD).
    Methods: We used high-throughput sequencing of small RNAs from human and mouse apoptotic primary macrophages, and analyzed the data by empirical Bayes moderated t-statistics to assess differential expression and the Benjamini and Hochberg method to control the false discovery rate. Results were then confirmed by Northern blot and RT-qPCR in foam cells and in two animal models for atherosclerosis, namely ApoE(-/-) and Ldlr(-/-) mouse lines. Quantitative RT-PCR to detect identified small RNAs, the RNY-derived small RNAs, was performed using sera of 263 patients with CAD compared to 514 matched healthy controls; the Student t-test was applied to statistically assess differences. Associations of small RNAs with clinical characteristics and biological markers were tested using Spearman's rank correlations, while multivariate logistic regressions were performed to test the statistical association of small RNA levels with CAD.
    Results: Here, we report that, in macrophages stimulated with pro-apoptotic or pro-atherogenic stimuli, the Ro-associated non-coding RNAs, called RNYs or Y-RNAs, are processed into small RNAs (~24-34 nt) referred to as small-RNYs (s-RNYs), including s-RNY1-5p processed from RNY1. A significant upregulation of s-RNY expression was found in aortic arches and blood plasma from ApoE(-/-) and Ldlr(-/-) mice and in serum from CAD patients (P <0.001). Biostatistical analysis revealed a positive association of s-RNY1-5p with hs-CRP and ApoB levels; however, no statistical interaction was found between either of these two markers and s-RNY1-5p in relation to the CAD status. Levels of s-RNY1-5p were also independent from statin and fibrate therapies.
    Conclusion: Our results position the s-RNY1-5p as a relevant novel independent diagnostic biomarker for atherosclerosis-related diseases. Measurement of circulating s-RNY expression would be a valuable companion diagnostic to monitor foam cell apoptosis during atherosclerosis pathogenesis and to evaluate patient's responsiveness to future therapeutic strategies aiming to attenuate apoptosis in foam cells in advanced atherosclerotic lesions.
    Mesh-Begriff(e) Aged ; Animals ; Aorta, Thoracic/metabolism ; Atherosclerosis/blood ; Biomarkers/blood ; Case-Control Studies ; Cell Line ; Coronary Artery Disease/blood ; Female ; High-Throughput Nucleotide Sequencing ; Humans ; Male ; Mice ; Mice, 129 Strain ; Mice, Inbred C57BL ; Mice, Knockout ; Middle Aged ; RNA, Untranslated/blood ; Sequence Analysis, RNA
    Chemische Substanzen Biomarkers ; RNA, Untranslated
    Sprache Englisch
    Erscheinungsdatum 2015-10-08
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 1741-7015
    ISSN (online) 1741-7015
    DOI 10.1186/s12916-015-0489-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

    Zusatzmaterialien

    Kategorien

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

    Fernleihe an ZB MED

    Sie können sich den gewünschten Titel als lokale Nutzerin oder lokaler Nutzer von ZB MED direkt an den Standort Köln schicken lassen.

  5. Artikel ; Online: The PRKAA1/AMPKα1 pathway triggers autophagy during CSF1-induced human monocyte differentiation and is a potential target in CMML.

    Obba, Sandrine / Hizir, Zoheir / Boyer, Laurent / Selimoglu-Buet, Dorothée / Pfeifer, Anja / Michel, Gregory / Hamouda, Mohamed-Amine / Gonçalvès, Diogo / Cerezo, Michael / Marchetti, Sandrine / Rocchi, Stephane / Droin, Nathalie / Cluzeau, Thomas / Robert, Guillaume / Luciano, Frederic / Robaye, Bernard / Foretz, Marc / Viollet, Benoit / Legros, Laurence /
    Solary, Eric / Auberger, Patrick / Jacquel, Arnaud

    Autophagy

    2015  Band 11, Heft 7, Seite(n) 1114–1129

    Abstract: Autophagy is induced during differentiation of human monocytes into macrophages that is mediated by CSF1/CSF-1/M-CSF (colony stimulating factor 1 [macrophage]). However, little is known about the molecular mechanisms that link CSF1 receptor engagement to ...

    Abstract Autophagy is induced during differentiation of human monocytes into macrophages that is mediated by CSF1/CSF-1/M-CSF (colony stimulating factor 1 [macrophage]). However, little is known about the molecular mechanisms that link CSF1 receptor engagement to the induction of autophagy. Here we show that the CAMKK2-PRKAA1-ULK1 pathway is required for CSF1-induced autophagy and human monocyte differentiation. We reveal that this pathway links P2RY6 to the induction of autophagy, and we decipher the signaling network that links the CSF1 receptor to P2RY6-mediated autophagy and monocyte differentiation. In addition, we show that the physiological P2RY6 ligand UDP and the specific P2RY6 agonist MRS2693 can restore normal monocyte differentiation through reinduction of autophagy in primary myeloid cells from some but not all chronic myelomonocytic leukemia (CMML) patients. Collectively, our findings highlight an essential role for PRKAA1-mediated autophagy during differentiation of human monocytes and pave the way for future therapeutic interventions for CMML.
    Mesh-Begriff(e) AMP-Activated Protein Kinases/metabolism ; Animals ; Autophagy/drug effects ; Calcium-Calmodulin-Dependent Protein Kinase Kinase/metabolism ; Cell Differentiation/drug effects ; Cell Line, Tumor ; Enzyme Activation/drug effects ; Humans ; Leukemia, Myeloid/enzymology ; Leukemia, Myeloid/pathology ; Macrophage Colony-Stimulating Factor/pharmacology ; Mice, Inbred C57BL ; Models, Biological ; Monocytes/cytology ; Monocytes/drug effects ; Monocytes/metabolism ; Phospholipase C gamma/metabolism ; Receptors, Purinergic P2/metabolism ; Signal Transduction/drug effects ; Uridine Diphosphate/pharmacology
    Chemische Substanzen Receptors, Purinergic P2 ; purinoceptor P2Y6 ; Uridine Diphosphate (58-98-0) ; Macrophage Colony-Stimulating Factor (81627-83-0) ; CAMKK2 protein, human (EC 2.7.11.17) ; Calcium-Calmodulin-Dependent Protein Kinase Kinase (EC 2.7.11.17) ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Phospholipase C gamma (EC 3.1.4.3)
    Sprache Englisch
    Erscheinungsdatum 2015
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2015.1034406
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

    Volltext online

    Zusatzmaterialien

    Kategorien

    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 6741: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Über subito bestellen

    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

Zum Seitenanfang