Endocytosis contributes to BMP2-induced Smad signalling and neuronal growth

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dc.contributor.author Hegarty, Shane V.
dc.contributor.author Sullivan, Aideen M.
dc.contributor.author O'Keefe, Gerard W.
dc.date.accessioned 2017-02-13T14:47:35Z
dc.date.available 2017-02-13T14:47:35Z
dc.date.issued 2017-02-08
dc.identifier.citation Hegarty, S. V., Sullivan, A. M. and O’Keeffe, G. W. 'Endocytosis contributes to BMP2-induced Smad signalling and neuronal growth', Neuroscience Letters. Article in Press. doi:10.1016/j.neulet.2017.02.013 en
dc.identifier.issn 0304-3940
dc.identifier.uri http://hdl.handle.net/10468/3622
dc.identifier.doi 10.1016/j.neulet.2017.02.013
dc.description.abstract Bone morphogenetic protein 2 (BMP2) is a neurotrophic factor which induces the growth of midbrain dopaminergic (DA) neurons in vitro and in vivo, and its neurotrophic effects have been shown to be dependent on activation of BMP receptors (BMPRs) and Smad 1/5/8 signalling. However, the precise intracellular cascades that regulate BMP2-BMPR-Smad-signalling-induced neurite growth remain unknown. Endocytosis has been shown to regulate Smad 1/5/8 signalling and differentiation induced by BMPs. However, these studies were carried out in non-neural cells. Indeed, there are scant reports regarding the role of endocytosis in BMP-Smad signalling in neurons. To address this, and to further characterise the mechanisms regulating the neurotrophic effects of BMP2, the present study examined the role of dynamin-dependent endocytosis in BMP2-induced Smad signalling and neurite growth in the SH-SY5Y neuronal cell line. The activation, temporal kinetics and magnitude of Smad 1/5/8 signalling induced by BMP2 were significantly attenuated by dynasore-mediated inhibition of endocytosis in SH-SY5Y cells. Furthermore, BMP2-induced increases in neurite length and neurite branching in SH-SY5Y cells were significantly reduced following inhibition of dynamin-dependent endocytosis using dynasore. This study demonstrates that BMP2-induced Smad signalling and neurite growth is regulated by dynamin-dependent endocytosis in a model of human midbrain dopaminergic neurons. en
dc.description.sponsorship Irish Research Council (R15897; SVH/AS/GOK); National University of Ireland (R16189; SVH/AS/GOK); Science Foundation Ireland (SFI under the Grant Number 15/CDA/13498) en
dc.format.mimetype application/pdf en
dc.language.iso en en
dc.publisher Elsevier en
dc.rights © 2017 Elsevier B.V. All rights reserved. This manuscript version is made available under the CC-BY-NC-ND 4.0 license. en
dc.rights.uri https://creativecommons.org/licenses/by-nc-nd/4.0/ en
dc.subject Endocytosis en
dc.subject BMP2 en
dc.subject Dynamin-dependent en
dc.subject Smad signalling en
dc.subject Neurite growth en
dc.title Endocytosis contributes to BMP2-induced Smad signalling and neuronal growth en
dc.type Article (peer-reviewed) en
dc.internal.authorcontactother Shane Hegarty, Department Of Anatomy & Neuroscience, University College Cork, Cork, Ireland. +353-21-490-3000 Email: shane.hegarty@ucc.ie en
dc.internal.availability Full text available en
dc.check.info Access to this item is restricted until 12 months after publication by the request of the publisher. en
dc.check.date 2018-02-08
dc.date.updated 2017-02-13T14:37:32Z
dc.description.version Accepted Version en
dc.internal.rssid 383418297
dc.contributor.funder Science Foundation Ireland en
dc.contributor.funder Irish Research Council en
dc.contributor.funder National University of Ireland en
dc.description.status Peer reviewed en
dc.identifier.journaltitle Neuroscience Letters en
dc.internal.copyrightchecked No !!CORA!! en
dc.internal.licenseacceptance Yes en
dc.internal.IRISemailaddress shane.hegarty@ucc.ie en
dc.internal.bibliocheck Article in Press Feb 2017. Update publication details, and citation (vol. page numbers etc) en


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© 2017 Elsevier B.V. All rights reserved. This manuscript version is made available under the CC-BY-NC-ND 4.0 license. Except where otherwise noted, this item's license is described as © 2017 Elsevier B.V. All rights reserved. This manuscript version is made available under the CC-BY-NC-ND 4.0 license.
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