يعرض 1 - 10 نتائج من 72 نتيجة بحث عن '"Paquin, Joanne"', وقت الاستعلام: 0.89s تنقيح النتائج
  1. 1
    دورية أكاديمية

    المساهمون: Perez, Mariela Gomez, Tanasie, Georgiana, Neree, Armelle Tchoumi, Suarez, Narjara Gonzalez, Lafortune, Clara, Paquin, Joanne, Marcocci, Lucia, Pietrangeli, Paola, Annabi, Borhane, Mateescu, Mircea Alexandru

    الوصف: Histamine is a biogenic amine implicated in various biological and pathological processes. Convenient cellular models are needed to screen and develop new antihistamine agents. This report aimed to characterize the response of neurons differentiated from mouse P19 embryonal carcinoma cells to histamine treatment, and to investigate the modulation of this response by antihistamine drugs, vegetal diamine oxidase, and catalase. The exposure of P19 neurons to histamine reduced cell viability to 65% maximally. This effect involves specific histamine receptors, since it was prevented by treatment with desloratadine and cimetidine, respectively, H-1 and H-2 antagonists, but not by the H-3 antagonist ciproxifan. RT-PCR analysis showed that P19 neurons express H-1 and H-2 receptors, and the H-3 receptor, although it seemed not involved in the histamine effect on these cells. The H-4 receptor was not expressed. H-1 and H-2 antagonists as well as vegetal diamine oxidase diminished the intracellular Ca2+ mobilization triggered by histamine. The treatment with vegetal diamine oxidase or catalase protected against mortality and a significant reduction of H2O2 level, generated from the cells under the histamine action, was found upon treatments with desloratadine, cimetidine, vegetal diamine oxidase, or catalase. Overall, the results indicate the expression of functional histamine receptors and open the possibility of using P19 neurons as model system to study the roles of histamine and related drugs in neuronal pathogenesis. This model is less expensive to operate and can be easily implemented by current laboratories of analysis and by Contract Research Organizations.

    العلاقة: info:eu-repo/semantics/altIdentifier/pmid/37171719; info:eu-repo/semantics/altIdentifier/wos/WOS:000986375300001; numberofpages:13; journal:AMINO ACIDS; https://hdl.handle.net/11573/1683040Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85159359004

  2. 2
    دورية أكاديمية

    المصدر: Proceedings of the National Academy of Sciences of the United States of America, 2004 Aug . 101(35), 13074-13079.

  3. 3
    دورية أكاديمية

    المصدر: Proceedings of the National Academy of Sciences of the United States of America, 2002 Jul 01. 99(14), 9550-9555.

  4. 4
    دورية أكاديمية

    المصدر: Amino Acids; Jun2023, Vol. 55 Issue 6, p821-833, 13p

    مستخلص: Histamine is a biogenic amine implicated in various biological and pathological processes. Convenient cellular models are needed to screen and develop new antihistamine agents. This report aimed to characterize the response of neurons differentiated from mouse P19 embryonal carcinoma cells to histamine treatment, and to investigate the modulation of this response by antihistamine drugs, vegetal diamine oxidase, and catalase. The exposure of P19 neurons to histamine reduced cell viability to 65% maximally. This effect involves specific histamine receptors, since it was prevented by treatment with desloratadine and cimetidine, respectively, H1 and H2 antagonists, but not by the H3 antagonist ciproxifan. RT-PCR analysis showed that P19 neurons express H1 and H2 receptors, and the H3 receptor, although it seemed not involved in the histamine effect on these cells. The H4 receptor was not expressed. H1 and H2 antagonists as well as vegetal diamine oxidase diminished the intracellular Ca2+ mobilization triggered by histamine. The treatment with vegetal diamine oxidase or catalase protected against mortality and a significant reduction of H2O2 level, generated from the cells under the histamine action, was found upon treatments with desloratadine, cimetidine, vegetal diamine oxidase, or catalase. Overall, the results indicate the expression of functional histamine receptors and open the possibility of using P19 neurons as model system to study the roles of histamine and related drugs in neuronal pathogenesis. This model is less expensive to operate and can be easily implemented by current laboratories of analysis and by Contract Research Organizations. [ABSTRACT FROM AUTHOR]

    : Copyright of Amino Acids is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

  5. 5
    رسالة جامعية
  6. 6
    دورية أكاديمية

    مصطلحات موضوعية: IN VITRO METHODS AND ALTERNATIVES TO ANIMALS

    الوصف: Atrazine and nitrogenous fertilizers are agrochemical contaminants frequently detected in water systems in North America. Several studies reported their ability to affect amphibian and mammalian development. Retinoids, supplied in the diet or synthesized by cells, are essential to embryogenesis. Disturbance of their homeostasis may lead to teratogenic effects. Retinoic acid (RA) is a major retinoid regulator of cell proliferation and differentiation. Previous studies reported alterations of retinoid stores in bullfrogs of Yamaska River subwatersheds (Québec, Canada), a region of intensive agricultural activities associated with atrazine, nitrate, and nitrite contaminants. These contaminants could affect RA metabolism and RA-mediated processes. Mouse P19 embryonic stem cells, which can differentiate to neurons in response to RA, were used to test this hypothesis. Cells were cultured in the absence or presence of contaminants during neuroinduction with RA and assayed by flow cytometry for expression of stage-specific embryonic antigen-1 (SSEA1) (embryonic marker) and βIII-tubulin (neuronal marker). Cell cultures were also analyzed for RA metabolism by high performance liquid chromotagraphy (HPLC). Downregulation of SSEA1 paralleled βIII-tubulin upregulation in an RA concentration–dependent manner. Atrazine, nitrate, and nitrite did not affect differentiation at environmentally encountered micromolar concentrations. However, low molar nitrite prevented RA-induced SSEA1 downregulation and decreased βIII-tubulin appearance. Decreased cell viability/proliferation accompanied these differentiation effects. P19 cells metabolized RA to polar retinoids. RA metabolism was not affected at any concentration of atrazine, nitrate, or nitrite. Environmentally relevant levels of these contaminants, thus, had no gross effect on neurodifferentiation and RA catabolism of embryonic stem cells. P19 cell–based bioassays may provide valuable tools in monitoring developmental toxicity.

    وصف الملف: text/html

  7. 7
    دورية أكاديمية

    مصطلحات موضوعية: In Vitro Toxicology and Alternative Testing

    الوصف: Atrazine and nitrogenous fertilizers are agrochemical contaminants frequently detected in water systems in North America. Several studies reported their ability to affect amphibian and mammalian development. Retinoids, supplied in the diet or synthesized by cells, are essential to embryogenesis. Disturbance of their homeostasis may lead to teratogenic effects. Retinoic acid (RA) is a major retinoid regulator of cell proliferation and differentiation. Previous studies reported alterations of retinoid stores in bullfrogs of Yamaska River subwatersheds (Québec, Canada), a region of intensive agricultural activities associated with atrazine, nitrate and nitrite contaminants. These contaminants could affect RA metabolism and RA-mediated processes. Mouse P19 embryonic stem cells, which can differentiate to neurons in response to RA, were used to test this hypothesis. Cells were cultured in the absence or presence of contaminants during neuroinduction with RA, and assayed by flow cytometry for expression of SSEA1 (embryonic marker) and βIII-tubulin (neuronal marker). Cell cultures were also analysed for RA metabolism by HPLC. Downregulation of SSEA1 paralleled βIII-tubulin upregulation in a RA concentration-dependent manner. Atrazine, nitrate and nitrite did not affect differentiation at environmentally-encountered micromolar concentrations. However, low molar nitrite prevented RA-induced SSEA1 downregulation, and decreased βIII-tubulin appearance. Decreased cell viability/proliferation accompanied these differentiation effects. P19 cells metabolized RA to polar retinoids. RA metabolism was not affected at any concentration of atrazine, nitrate or nitrite. Environmentally-relevant levels of these contaminants thus had no gross effect on neurodifferentiation and RA catabolism of embryonic stem cells. P19 cell-based bioassays may provide valuable tools in monitoring developmental toxicity.

    وصف الملف: text/html

  8. 8
    دورية أكاديمية

    المصدر: Journal of Neurochemistry ; volume 98, issue 3, page 838-850 ; ISSN 0022-3042 1471-4159

    الوصف: Neural apoptosis‐regulated convertase‐1/proprotein convertase subtilisin‐kexin like‐9 (NARC‐1/PCSK9) is a proprotein convertase recently described to play a major role in cholesterol homeostasis through enhanced degradation of the low‐density lipoprotein receptor (LDLR) and possibly in neural development. Herein, we investigated the potential involvement of this proteinase in the development of the CNS using mouse embryonal pluripotent P19 cells and the zebrafish as models. Time course quantitative RT–PCR analyses were performed following retinoic acid (RA)‐induced neuroectodermal differentiation of P19 cells. Accordingly, the mRNA levels of NARC‐1/PCSK9 peaked at day 2 of differentiation and fell off thereafter. In contrast, the expression of the proprotein convertases subtilisin kexin isozyme 1/site 1 protease and Furin was unaffected by RA, whereas that of PC5/6 and PC2 increased within and/or after the first 4 days of the differentiation period respectively. This pattern was not affected by the cholesterogenic transcription factor sterol regulatory element‐binding protein‐2, which normally up‐regulates NARC‐1/PCSK9 mRNA levels in liver. Furthermore, in P19 cells, RA treatment did not affect the protein level of the endogenous LDLR. This agrees with the unique expression pattern of NARC‐1/PCSK9 in the rodent CNS, including the cerebellum, where the LDLR is not significantly expressed. Whole‐mount in situ hybridization revealed that the pattern of expression of zebrafish NARC‐1/PCSK9 is similar to that of mouse both in the CNS and periphery. Specific knockdown of zebrafish NARC‐1/PCSK9 mRNA resulted in a general disorganization of cerebellar neurons and loss of hindbrain–midbrain boundaries, leading to embryonic death at ∼ 96 h after fertilization. These data support a novel role for NARC‐1/PCSK9 in CNS development, distinct from that in cholesterogenic organs such as liver.

  9. 9
    دورية أكاديمية

    المصدر: Stem Cells ; volume 25, issue 3, page 679-688 ; ISSN 1066-5099 1549-4918

    الوصف: Oxytocin (OT), a hormone recently identified in the heart, induces embryonic and cardiac somatic stem cells to differentiate into cardiomyocytes (CM), possibly through nitric oxide (NO). We verified this hypothesis using P19 cells and P19 Clone 6 derivatives expressing a green fluorescent protein (GFP) reporter linked to cardiac myosin light chain-2v promoter. OT treatment of these cells induced beating cell colonies that were fully inhibited by N,G-nitro-l-arginine-methyl-ester (l-NAME), an inhibitor of NO synthases (NOS), partially reduced by 1400W, an inhibitor of inducible NOS, and ODQ, an inhibitor of NO-sensitive guanylyl cyclases. The NO generator S-nitroso-N-acetylpenicillamine (SNAP) reversed the l-NAME inhibition of cell beating and GFP expression. In OT-induced cells, l-NAME significantly decreased transcripts of the cardiac markers Nkx2.5, MEF2c, α-myosin heavy chain, and less, GATA4, endothelial NOS, and atrial natriuretic peptide, as well as the skeletal myocyte (SM) marker myogenin. Image analysis of OT-induced P19Cl6-GFP cells revealed ventricular CM coexpressing sarcomeric α-actinin and GFP, with some cells exclusively expressing α-actinin, most likely of the SM phenotype. The OT-mediated production of CM, but not SM, was diminished by l-NAME. In P19 cells, exogenously added OT stimulated the expression of its own transcript, which was reduced in the presence of l-NAME. Surprisingly, l-NAME alone decreased the expression of anti-stage specific embryonic antigen-1 marker of the undifferentiated state and induced some beating colonies as well as GFP in P19Cl6-GFP cells. Collectively, our data suggest that the pleiotropic action of NO is involved in the initiation of CM differentiation of P19 cells and maintenance of their undifferentiated state.

  10. 10
    Patent

    مستخلص: The invention relates to oxytocin and oxytocin-related compounds and functional derivatives thereof, and uses thereof to induce differentiation of a non-cardiomyocyte (e.g. a stem/progenitor cell) to a cardiomyocyte. The invention further relates to the methods of prevention or treatment of conditions characterized by or associated with a cardiomyocyte loss or deficiency, by administration of oxytocin or an oxytocin-related compound or a functional derivative thereof to a subject, or via the administration/transplantation of a cell differentiated ex vivo by a method of the invention. The invention further relates to methods, uses, commercial packages and culture media relating to such differentiation and prevention/treatment.