<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-09-24T01:37:00Z</responseDate><request verb="GetRecord" identifier="oai:ruor.uottawa.ca:10393/4475" metadataPrefix="oai_dc">https://ruor.uottawa.ca/server/oai/request</request><GetRecord><record><header><identifier>oai:ruor.uottawa.ca:10393/4475</identifier><datestamp>2024-02-23T09:06:50Z</datestamp><setSpec>com_10393_242</setSpec><setSpec>col_10393_244</setSpec></header><metadata><oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
   <dc:title>Molecular regulation of neuronal apoptosis in PC12 cells.</dc:title>
   <dc:creator>Sridhar, Srikala.</dc:creator>
   <dc:contributor>Tenniswood, M.,</dc:contributor>
   <dc:subject>Biology, Molecular.</dc:subject>
   <dc:description>In this study apoptosis was induced in neuronal PC12 cells by 2-5 $\mu$M VM26 (teniposide, a known apoptotic inducer) and changes in the expression of genes considered to be involved in apoptosis were examined by RT-PCR. Cell death, DNA fragmentation and morphological changes associated with apoptosis were evident within 8 hours after exposure to VM26 indicating that VM26 is capable of inducing apoptosis. Within 8 hours of VM26 exposure, clusterin (TRPM-2) and IGFBP2 (Insulin-like growth factor binding protein 2) were both upregulated by 3 and 4 fold respectively. Cathepsin B (RSG-2) and RSG-3 (embigin) exhibited marginal changes in expression, only about 1.2 fold, over the 24 hour time course. Finally, IGFBP5 (Insulin-like growth factor binding protein 5) displayed a substantial decrease in expression, with a 4 fold decrease compared to control. Since IGFBPs appear to play a role in apoptosis, the effects of IGF-I treatment on cells undergoing apoptosis was examined. Treatment with IGF-I led to a dose-dependent protective effect on apoptosis induced by VM26. In the presence of 200 ng/ml IGF-I, cell viability was 52.1% at 24 hours compared to non-treated cells, at 35.8% viability. In addition, IGF-I was able to modulate cell viability, in a manner that did not involve induction of proliferation as assessed by cell counts in IGF-I treated and untreated PC12 cells. (Abstract shortened by UMI.)</dc:description>
   <dc:date>2009-03-19T14:13:16Z</dc:date>
   <dc:date>2009-03-19T14:13:16Z</dc:date>
   <dc:date>1997</dc:date>
   <dc:date>1997</dc:date>
   <dc:type>Thesis</dc:type>
   <dc:identifier>Source: Masters Abstracts International, Volume: 36-02, page: 0546.</dc:identifier>
   <dc:identifier>9780612220188</dc:identifier>
   <dc:identifier>http://hdl.handle.net/10393/4475</dc:identifier>
   <dc:identifier>http://dx.doi.org/10.20381/ruor-13875</dc:identifier>
   <dc:format>93 p.</dc:format>
   <dc:format>application/pdf</dc:format>
   <dc:publisher>University of Ottawa (Canada)</dc:publisher>
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