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    <datestamp>2012-04-27 12:03:14</datestamp>
    <lastmod>2019-01-17 15:36:46</lastmod>
    <status_changed>2012-04-27 12:03:14</status_changed>
    <type>thesis</type>
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    <creators>
      <item>
        <name>
          <family>Gale</family>
          <given>Zoe</given>
        </name>
      </item>
    </creators>
    <supervisors>
      <item>
        <name>
          <family>Scheven</family>
          <given>Ben</given>
        </name>
      </item>
      <item>
        <name>
          <family>Cooper</family>
          <given>Paul</given>
        </name>
      </item>
    </supervisors>
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      <item>University of Birmingham</item>
    </corp_creators>
    <title>Glial cell line-derived neurotrophic factor effects on dental pulp cells and osteoblast-like cells</title>
    <ispublished>unpub</ispublished>
    <subjects>
      <item>QR</item>
      <item>RK</item>
    </subjects>
    <divisions>10col_mede</divisions>
    <note>Published articles related to this research are available at:
http://eprints.bham.ac.uk/1141/ 
http://eprints.bham.ac.uk/1142/  

</note>
    <abstract>Glial cell line-derived neurotrophic factor (GDNF) is a growth factor promoting survival, proliferation and differentiation of neural crest cells. Neural crest cells play an important role within mesenchymal tissues during dental pulp and calvarial bone development. GDNF also has a role within non-neuronal tissues and is expressed during dental development. GDNF null mutations prevent the formation of the mineralised hard tissues of the tooth. The hypothesis for this study was that GDNF affects mesenchymal dental pulp cells (DPC), promoting the regenerative responses of mineralised tissues. This study utilised cell culture models to investigate the direct effects of GDNF on the proliferation and differentiation of dental pulp cells, bone marrow mesenchymal stromal/stem cells (BMSC) and calvarial osteoblasts. This research demonstrated that these culture models expressed GDNF and its receptors GFR\(\alpha\)1 and RET. GDNF was shown to directly stimulate DPC and osteoblast-like cell proliferation and differentiation. Moreover, GDNF was cytoprotective when DPCs were cultured under conditions reflecting aspects of inflammation, which may occur during repair. These conditions included supplementation with the pro-inflammatory cytokine TNF\(\alpha\) and culture under serum-starved conditions. It is proposed that GDNF may play an important regulatory role in dental pulp homeostasis and bone metabolism. </abstract>
    <date>2012-12</date>
    <date_tp>2011-12</date_tp>
    <date_type>graduation</date_type>
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    <ub_doc_source_spot>unchecked</ub_doc_source_spot>
    <copyright_status>This unpublished thesis/dissertation is copyright of the author and/or third parties.
The intellectual property rights of the author or third parties in respect of this work are as defined by The Copyright Designs and Patents Act 1988 or as modified by any successor legislation.  Any use made of information contained in this thesis/dissertation must be in accordance with that legislation and must be properly acknowledged.
Further distribution or reproduction in any format is prohibited without the permission of the copyright holder.</copyright_status>
    <other_funders>
      <item>The University of Birmingham</item>
    </other_funders>
    <full_text_status>public</full_text_status>
    <pages>265</pages>
    <institution>University of Birmingham</institution>
    <department>School of Dentistry</department>
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      <item>other</item>
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