{"id":{"repo_id":"ottawa-retro","oai_identifier":"oai:ruor.uottawa.ca:10393/4475"},"canonical_url":"https://search.dev.ndltd.org/etd/ottawa-retro/oai:ruor.uottawa.ca:10393/4475","repository":{"repo_id":"ottawa-retro","name":"University of Ottawa","base_url":"https://ruor.uottawa.ca/server/oai/request"},"display":{"title":"Molecular regulation of neuronal apoptosis in PC12 cells.","abstract":"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.)","abstract_html":"In this study apoptosis was induced in neuronal PC12 cells by 2-5 <span class=\"etd-inline-math\">&mu;</span>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.)","abstract_has_math":true,"creators":["Sridhar, Srikala."],"institution":"University of Ottawa (Canada)","degree_name":null,"degree_level":null,"degree_discipline":null,"degree_department":null,"school":null,"contributors":["Tenniswood, M.,"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2009,"date_issued":"2009-03-19T14:13:16Z","date_published":"2009-03-19T14:13:16Z","updated_at":"2026-07-24T03:39:31Z","subjects":["Biology, Molecular."],"languages":[],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["Source: Masters Abstracts International, Volume: 36-02, page: 0546.","9780612220188","http://dx.doi.org/10.20381/ruor-13875"],"render_values":[{"text":"Source: Masters Abstracts International, Volume: 36-02, page: 0546.","href":null,"code":true},{"text":"9780612220188","href":null,"code":true},{"text":"http://dx.doi.org/10.20381/ruor-13875","href":"http://dx.doi.org/10.20381/ruor-13875","code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/10393/4475","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Tenniswood, M.,"]},{"key":"dc:creator","label":"Author","values":["Sridhar, Srikala."]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2009-03-19T14:13:16Z","1997"]},{"key":"dc:publisher","label":"Institution","values":["University of Ottawa (Canada)"]},{"key":"dc:type","label":"Dc Type","values":["Thesis"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Molecular."]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["Source: Masters Abstracts International, Volume: 36-02, page: 0546.","9780612220188","http://hdl.handle.net/10393/4475","http://dx.doi.org/10.20381/ruor-13875"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["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.)"]},{"key":"dc:format","label":"Dc Format","values":["93 p.","application/pdf"]},{"key":"dc:title","label":"Title","values":["Molecular regulation of neuronal apoptosis in PC12 cells."]}]}],"canonical_facts":{"dc:contributor":["Tenniswood, M.,"],"dc:creator":["Sridhar, Srikala."],"dc:date":["2009-03-19T14:13:16Z","1997"],"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:format":["93 p.","application/pdf"],"dc:identifier":["Source: Masters Abstracts International, Volume: 36-02, page: 0546.","9780612220188","http://hdl.handle.net/10393/4475","http://dx.doi.org/10.20381/ruor-13875"],"dc:publisher":["University of Ottawa (Canada)"],"dc:subject":["Biology, Molecular."],"dc:title":["Molecular regulation of neuronal apoptosis in PC12 cells."],"dc:type":["Thesis"]},"updated_at":"2026-07-24T03:39:31Z"}