Molecular regulation of neuronal apoptosis in PC12 cells.
type: CreativeWork
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.)
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.)
author: Sridhar, Srikala.
keywords: Biology, Molecular.
identifier: Source: Masters Abstracts International, Volume: 36-02, page: 0546.
date published: 2009-03-19T14:13:16Z
date modified: 2026-07-24T03:39:31Z
provider: University of Ottawa
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: University of Ottawa (Canada)

PropertyValue
property ID: Handle
value: http://hdl.handle.net/10393/4475

PropertyValue
property ID: DOI
value: 10.20381/ruor-13875