{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/86759"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/86759","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Angiotensin II Modulation of NMDA Receptor Function: Characterization of Mechanisms Attenuating Excitotoxicity in Neurons","abstract":"In the last study, we investigated the involvement of Bcl-2 in the suppression of NMDA-mediated neurotoxicity by Ang II. The viability of differentiated N1E and NG108 neuronal cell lines was reduced following exposure to NMDA in a dose-dependent manner. Excitotoxicity in N1E cells was inhibited by the noncompetitive NMDA receptor antagonist, MK-801. Further, NMDA receptor-mediated cell death was attenuated by Ang II in NG108 cells. A concentration-dependent decrease in intracellular Bcl-2 protein levels was observed following treatment with NMDA, and this reduction was inhibited by MK801. Addition of Ang II suppressed the NMDA receptor-mediated reduction in Bcl-2. The Ang II effect on NMDA-mediated changes in Bcl-2 expression was blocked by PD 123319, but was not significantly altered by losartan. Taken together, these results suggest that the decrease in Bcl-2 expression induced by NMDA is attenuated by AT2 activation. (Abstract shortened by UMI.).","abstract_html":"In the last study, we investigated the involvement of Bcl-2 in the suppression of NMDA-mediated neurotoxicity by Ang II. The viability of differentiated N1E and NG108 neuronal cell lines was reduced following exposure to NMDA in a dose-dependent manner. Excitotoxicity in N1E cells was inhibited by the noncompetitive NMDA receptor antagonist, MK-801. Further, NMDA receptor-mediated cell death was attenuated by Ang II in NG108 cells. A concentration-dependent decrease in intracellular Bcl-2 protein levels was observed following treatment with NMDA, and this reduction was inhibited by MK801. Addition of Ang II suppressed the NMDA receptor-mediated reduction in Bcl-2. The Ang II effect on NMDA-mediated changes in Bcl-2 expression was blocked by PD 123319, but was not significantly altered by losartan. Taken together, these results suggest that the decrease in Bcl-2 expression induced by NMDA is attenuated by AT2 activation. (Abstract shortened by UMI.).","abstract_has_math":false,"creators":["Schelman, William Russell"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Microbiology","degree_department":null,"school":null,"contributors":["Weyhenmeyer, James A."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-28T15:17:52Z","date_published":"2015-09-28T15:17:52Z","updated_at":"2026-07-22T22:26:27Z","subjects":["Biology, Molecular"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI9971184"],"render_values":[{"text":"(MiAaPQ)AAI9971184","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/86759","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Weyhenmeyer, James A."]},{"key":"dc:creator","label":"Author","values":["Schelman, William Russell"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-28T15:17:52Z","10000-01-01","2000"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Microbiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Molecular"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/86759","(MiAaPQ)AAI9971184"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["In the last study, we investigated the involvement of Bcl-2 in the suppression of NMDA-mediated neurotoxicity by Ang II. The viability of differentiated N1E and NG108 neuronal cell lines was reduced following exposure to NMDA in a dose-dependent manner. Excitotoxicity in N1E cells was inhibited by the noncompetitive NMDA receptor antagonist, MK-801. Further, NMDA receptor-mediated cell death was attenuated by Ang II in NG108 cells. A concentration-dependent decrease in intracellular Bcl-2 protein levels was observed following treatment with NMDA, and this reduction was inhibited by MK801. Addition of Ang II suppressed the NMDA receptor-mediated reduction in Bcl-2. The Ang II effect on NMDA-mediated changes in Bcl-2 expression was blocked by PD 123319, but was not significantly altered by losartan. Taken together, these results suggest that the decrease in Bcl-2 expression induced by NMDA is attenuated by AT2 activation. (Abstract shortened by UMI.).","Made available in DSpace on 2015-09-28T15:17:52Z (GMT). No. of bitstreams: 2 license.txt: 4848 bytes, checksum: 96035ab3f5e1c23cc7138a224ce498bd (MD5) 9971184.pdf: 8159815 bytes, checksum: 2e39d64bec99412f433ccbccf704ef66 (MD5) Previous issue date: 2000","Embargo set by: Seth Robbins for item 88040 Lift date: Forever Reason: Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","Restricted to the U of I community idenfinitely during batch ingest of legacy ETDs","U of I Only","138 p.","Thesis (Ph.D.)--University of Illinois at Urbana-Champaign, 2000."]},{"key":"dc:title","label":"Title","values":["Angiotensin II Modulation of NMDA Receptor Function: Characterization of Mechanisms Attenuating Excitotoxicity in Neurons"]}]}],"canonical_facts":{"dc:contributor":["Weyhenmeyer, James A."],"dc:creator":["Schelman, William Russell"],"dc:date":["2015-09-28T15:17:52Z","10000-01-01","2000"],"dc:description":["In the last study, we investigated the involvement of Bcl-2 in the suppression of NMDA-mediated neurotoxicity by Ang II. The viability of differentiated N1E and NG108 neuronal cell lines was reduced following exposure to NMDA in a dose-dependent manner. Excitotoxicity in N1E cells was inhibited by the noncompetitive NMDA receptor antagonist, MK-801. Further, NMDA receptor-mediated cell death was attenuated by Ang II in NG108 cells. A concentration-dependent decrease in intracellular Bcl-2 protein levels was observed following treatment with NMDA, and this reduction was inhibited by MK801. Addition of Ang II suppressed the NMDA receptor-mediated reduction in Bcl-2. The Ang II effect on NMDA-mediated changes in Bcl-2 expression was blocked by PD 123319, but was not significantly altered by losartan. Taken together, these results suggest that the decrease in Bcl-2 expression induced by NMDA is attenuated by AT2 activation. (Abstract shortened by UMI.).","Made available in DSpace on 2015-09-28T15:17:52Z (GMT). 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