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Conference Paper: Dichotomic role of NAADP/two-pore channel 2/Ca2+ signaling in regulating neural differentiation of mouse embryonic stem cells

TitleDichotomic role of NAADP/two-pore channel 2/Ca2+ signaling in regulating neural differentiation of mouse embryonic stem cells
Authors
Issue Date2011
PublisherThe American Society for Cell Biology. The Conference's website is located at http://ascb.org/index.php?option=com_content&view=article&id=745&Itemid=305
Citation
The 51th Annual Meeting of the American Society for Cell Biology (ASCB), Denver CO., 11-15 December 2011. In Regular Abstracts, 2011, p. 1059, abstract no. 1866 How to Cite?
AbstractThe mobilization of intracellular Ca2+stores is involved in diverse cellular functions, including cell proliferation and differentiation. At least three endogenous Ca2+mobilizing messengers have been identified, including inositol trisphosphate (IP3), cyclic adenosine diphosphoribose (cADPR), and nicotinic adenine acid dinucleotide phosphate (NAADP). Similar to IP3, NAADP can mobilize calcium release in a wide variety of cell types and species, from plants to animals. Moreover, it has been previously shown that NAADP but not IP3-mediated Ca2+increases can potently induce neuronal differentiation in PC12 cells. Recently, two pore channels (TPCs) have been identified as a novel family of NAADP-gated calcium release channels in endolysosome. Therefore, it is of great interest to examine the role of TPC2 in the neural differentiation of mouse ES cells. We found that the expression of TPC2 is markedly decreased during the initial ES cell entry into neural progenitors, and the levels of TPC2 gradually rebound during the late stages of neurogenesis. Correspondingly, perturbing the NAADP signaling by TPC2 knockdown accelerates mouse ES cell differentiation into neural progenitors but inhibits these neural progenitors from committing to the final neural lineage. Interestingly, TPC2 knockdown has no effect on the differentiation of astrocytes and oligodendrocytes of mouse ES cells. Overexpression of TPC2, on the other hand, inhibits mouse ES cell from entering the neural lineage. Taken together, our data indicate that the NAADP/TPC2-mediated Ca2+signaling pathway plays a temporal and dichotomic role in modulating the neural lineage entry of ES cells; in that NAADP signaling antagonizes ES cell entry to early neural progenitors, but promotes late neural differentiation.
DescriptionPoster Presentation - Stem Cells and Pluripotency: abstract no. 1866
Persistent Identifierhttp://hdl.handle.net/10722/165579

 

DC FieldValueLanguage
dc.contributor.authorZhang, Zen_US
dc.contributor.authorYue, J-
dc.date.accessioned2012-09-20T08:20:12Z-
dc.date.available2012-09-20T08:20:12Z-
dc.date.issued2011en_US
dc.identifier.citationThe 51th Annual Meeting of the American Society for Cell Biology (ASCB), Denver CO., 11-15 December 2011. In Regular Abstracts, 2011, p. 1059, abstract no. 1866en_US
dc.identifier.urihttp://hdl.handle.net/10722/165579-
dc.descriptionPoster Presentation - Stem Cells and Pluripotency: abstract no. 1866-
dc.description.abstractThe mobilization of intracellular Ca2+stores is involved in diverse cellular functions, including cell proliferation and differentiation. At least three endogenous Ca2+mobilizing messengers have been identified, including inositol trisphosphate (IP3), cyclic adenosine diphosphoribose (cADPR), and nicotinic adenine acid dinucleotide phosphate (NAADP). Similar to IP3, NAADP can mobilize calcium release in a wide variety of cell types and species, from plants to animals. Moreover, it has been previously shown that NAADP but not IP3-mediated Ca2+increases can potently induce neuronal differentiation in PC12 cells. Recently, two pore channels (TPCs) have been identified as a novel family of NAADP-gated calcium release channels in endolysosome. Therefore, it is of great interest to examine the role of TPC2 in the neural differentiation of mouse ES cells. We found that the expression of TPC2 is markedly decreased during the initial ES cell entry into neural progenitors, and the levels of TPC2 gradually rebound during the late stages of neurogenesis. Correspondingly, perturbing the NAADP signaling by TPC2 knockdown accelerates mouse ES cell differentiation into neural progenitors but inhibits these neural progenitors from committing to the final neural lineage. Interestingly, TPC2 knockdown has no effect on the differentiation of astrocytes and oligodendrocytes of mouse ES cells. Overexpression of TPC2, on the other hand, inhibits mouse ES cell from entering the neural lineage. Taken together, our data indicate that the NAADP/TPC2-mediated Ca2+signaling pathway plays a temporal and dichotomic role in modulating the neural lineage entry of ES cells; in that NAADP signaling antagonizes ES cell entry to early neural progenitors, but promotes late neural differentiation.-
dc.languageengen_US
dc.publisherThe American Society for Cell Biology. The Conference's website is located at http://ascb.org/index.php?option=com_content&view=article&id=745&Itemid=305-
dc.relation.ispartof51th ASCB Annual Meeting 2011en_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.titleDichotomic role of NAADP/two-pore channel 2/Ca2+ signaling in regulating neural differentiation of mouse embryonic stem cellsen_US
dc.typeConference_Paperen_US
dc.identifier.emailYue, J: jyue@hku.hken_US
dc.identifier.authorityYue, J=rp00286en_US
dc.description.naturepostprint-
dc.identifier.hkuros208769en_US
dc.identifier.volumeRegular Abstracts-
dc.identifier.spage1059-
dc.identifier.epage1059-
dc.publisher.placeUnited States-

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