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  1. Article ; Online: Endothelial-to-Mesenchymal Transition in Cancer

    Nicolas Clere / Sarah Renault / Isabelle Corre

    Frontiers in Cell and Developmental Biology, Vol

    2020  Volume 8

    Abstract: Cancer is one of the most important causes of morbidity and mortality worldwide. Tumor cells grow in a complex microenvironment constituted of immune, stromal, and vascular cells that supports growth, angiogenesis, and metastasis. Endothelial cells (ECs) ...

    Abstract Cancer is one of the most important causes of morbidity and mortality worldwide. Tumor cells grow in a complex microenvironment constituted of immune, stromal, and vascular cells that supports growth, angiogenesis, and metastasis. Endothelial cells (ECs) are major components of the vascular microenvironment. These cells have been described for their plasticity and potential to transdifferentiate into mesenchymal cells through a process known as endothelial-to-mesenchymal transition (EndMT). This complex process is controlled by various factors, by which ECs convert into a phenotype characterized by mesenchymal protein expression and motile, contractile morphology. Initially described in normal heart development, EndMT is now identified in several pathologies, and especially in cancer. In this review, we highlight the process of EndMT in the context of cancer and we discuss it as an important adaptive process of the tumor microenvironment that favors tumor growth and dissemination but also resistance to treatment. Thus, we underline targeting of EndMT as a potential therapeutic strategy.
    Keywords endothelial ; mesenchymal ; plasticity ; cancer ; CAF ; metastasis ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2020-08-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article: Two dechlorinated chlordecone derivatives formed by in situ chemical reduction are devoid of genotoxicity and mutagenicity and have lower proangiogenic properties compared to the parent compound

    Legeay, Samuel / Christophe Mouvet / Fabrice Nesslany / Nicolas Clere / Pierre-André Billat / Sébastien Bristeau / Sébastien Faure

    Environmental science and pollution research international. 2018 May, v. 25, no. 15

    2018  

    Abstract: Chlordecone (CLD) is a chlorinated hydrocarbon insecticide, now classified as a persistent organic pollutant. Several studies have previously reported that chronic exposure to CLD leads to hepatotoxicity, neurotoxicity, raises early child development and ...

    Abstract Chlordecone (CLD) is a chlorinated hydrocarbon insecticide, now classified as a persistent organic pollutant. Several studies have previously reported that chronic exposure to CLD leads to hepatotoxicity, neurotoxicity, raises early child development and pregnancy complications, and increases the risk of liver and prostate cancer. In situ chemical reduction (ISCR) has been identified as a possible way for the remediation of soils contaminated by CLD. In the present study, the objectives were (i) to evaluate the genotoxicity and the mutagenicity of two CLD metabolites formed by ISCR, CLD-5a-hydro, or CLD-5-hydro (5a- or 5- according to CAS nomenclature; CLD-1Cl) and tri-hydroCLD (CLD-3Cl), and (ii) to explore the angiogenic properties of these molecules. Mutagenicity and genotoxicity were investigated using the Ames’s technique on Salmonella typhimurium and the in vitro micronucleus micromethod with TK6 human lymphoblastoid cells. The proangiogenic properties were evaluated on the in vitro capillary network formation of human primary endothelial cells. Like CLD, the dechlorinated derivatives of CLD studied were devoid of genotoxic and mutagenic activity. In the assay targeting angiogenic properties, significantly lower microvessel lengths formed by endothelial cells were observed for the CLD-3Cl-treated cells compared to the CLD-treated cells for two of the three tested concentrations. These results suggest that dechlorinated CLD derivatives are devoid of mutagenicity and genotoxicity and have lower proangiogenic properties than CLD.
    Keywords chemical reduction ; child development ; chlordecone ; chronic exposure ; endothelial cells ; genotoxicity ; hepatotoxicity ; liver ; metabolites ; mutagenicity ; mutagens ; neurotoxicity ; polluted soils ; pregnancy complications ; prostatic neoplasms ; remediation ; risk ; Salmonella Typhimurium
    Language English
    Dates of publication 2018-05
    Size p. 14313-14323.
    Publishing place Springer Berlin Heidelberg
    Document type Article
    ZDB-ID 1178791-0
    ISSN 1614-7499 ; 0944-1344
    ISSN (online) 1614-7499
    ISSN 0944-1344
    DOI 10.1007/s11356-017-8592-6
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 5915: Show issues

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  3. Article ; Online: Estrogen receptor α/HDAC/NFAT axis for delphinidin effects on proliferation and differentiation of T lymphocytes from patients with cardiovascular risks

    Ousama Dayoub / Soazig Le Lay / Raffaella Soleti / Nicolas Clere / Gregory Hilairet / Séverine Dubois / Frédéric Gagnadoux / Jérôme Boursier / Maria Carmen Martínez / Ramaroson Andriantsitohaina

    Scientific Reports, Vol 7, Iss 1, Pp 1-

    2017  Volume 17

    Abstract: Abstract Delphinidin, an anthocyanin present in red wine, has been reported to preserve the integrity of endothelium via an estrogen receptor alpha (ERα)-dependent mechanism. However, the effect of delphinidin on the immune response in obesity-related ... ...

    Abstract Abstract Delphinidin, an anthocyanin present in red wine, has been reported to preserve the integrity of endothelium via an estrogen receptor alpha (ERα)-dependent mechanism. However, the effect of delphinidin on the immune response in obesity-related inflammation remains unknown. Given the important role of T lymphocytes in obesity-related inflammation, we investigated the effect of delphinidin on proliferation and differentiation of T lymphocytes from healthy subjects and metabolic syndrome patients. Delphinidin decreased the proliferation stimulated by different agents acting through different mechanisms. This effect of delphinidin was associated with its ability to inhibit Ca2+ signaling via reduced store-operated Ca2+ entry and release, and subsequent decrease of HDAC and NFAT activations. Delphinidin also inhibited ERK1/2 activation. Pharmacological inhibition of ER with fulvestrant, or deletion of ERα, prevented the effect of delphinidin. Further, delphinidin suppressed the differentiation of T cells toward Th1, Th17 and Treg without affecting Th2 subsets. Interestingly, delphinidin inhibited both proliferation and differentiation of T cells taken from patients with cardiovascular risks associated with metabolic syndrome. Together, we propose that delphinidin, by acting on ERα via multiple cellular targets, may represent a new approach against chronic inflammation associated with T lymphocyte activation, proliferation and differentiation, in patients with cardiovascular risk factors.
    Keywords Medicine ; R ; Science ; Q
    Subject code 616
    Language English
    Publishing date 2017-08-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article: Mycobacterial Toxin Induces Analgesia in Buruli Ulcer by Targeting the Angiotensin Pathways

    Marion, Estelle / Ok-Ryul Song / Thierry Christophe / Jérémie Babonneau / Denis Fenistein / Joël Eyer / Frank Letournel / Daniel Henrion / Nicolas Clere / Vincent Paille / Nathalie C. Guérineau / Jean-Paul Saint André / Philipp Gersbach / Karl-Heinz Altmann / Timothy Paul Stinear / Yannick Comoglio / Guillaume Sandoz / Laurence Preisser / Yves Delneste /
    Edouard Yeramian / Laurent Marsollier / Priscille Brodin

    Cell. 2014 June 19, v. 157

    2014  

    Abstract: Mycobacterium ulcerans, the etiological agent of Buruli ulcer, causes extensive skin lesions, which despite their severity are not accompanied by pain. It was previously thought that this remarkable analgesia is ensured by direct nerve cell destruction. ... ...

    Abstract Mycobacterium ulcerans, the etiological agent of Buruli ulcer, causes extensive skin lesions, which despite their severity are not accompanied by pain. It was previously thought that this remarkable analgesia is ensured by direct nerve cell destruction. We demonstrate here that M. ulcerans-induced hypoesthesia is instead achieved through a specific neurological pathway triggered by the secreted mycobacterial polyketide mycolactone. We decipher this pathway at the molecular level, showing that mycolactone elicits signaling through type 2 angiotensin II receptors (AT2Rs), leading to potassium-dependent hyperpolarization of neurons. We further validate the physiological relevance of this mechanism with in vivo studies of pain sensitivity in mice infected with M. ulcerans, following the disruption of the identified pathway. Our findings shed new light on molecular mechanisms evolved by natural systems for the induction of very effective analgesia, opening up the prospect of new families of analgesics derived from such systems.
    Keywords Mycobacterium ulcerans ; analgesia ; analgesics ; angiotensin II ; etiological agents ; in vivo studies ; mice ; neurons ; pain ; pain assessment ; receptors ; skin lesions ; somatosensory disorders
    Language English
    Dates of publication 2014-0619
    Size p. 1565-1576.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2014.04.040
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

    Z 75/702: Show issues
    Z 93: Show issues

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