{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/84794"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/84794","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Modulators of Inflammation and Steroid Receptors Regulate Proteinase Inhibitor 9 Gene Expression","abstract":"In addition to pro-inflammatory agents, the synthetic anti-inflammatory glucocorticoid, dexamethasone, induced PI-9 gene expression via an imperfect glucocorticoid response element (GRE) located at -208. Dexamethasone induced PI-9 mRNA and protein. Dexamethasone-glucocorticoid receptor (GR) complex inhibited IL-1beta induced PI-9 gene expression but IL-1beta did not interfere with dexamethasone induction of PI-9. Glucocorticoid administration resulted in reduced p65 binding to a consensus NF-kappaB element. To investigate the mechanism of crosstalk between Dex-GR and NF-kappaB, we analyzed the effect of dexamethasone on induction of IkappaB-alpha, the inhibitory heterodimer of p65. Dexamethasone induced IkappaBalpha in HepG2 cells. This may be one of the mechanisms used by Dex-GR to interfere with NF-kappaB activity and block IL-1beta-induced PI-9 gene expression. Our findings show that liganded GR may regulate IL-1beta induction of PI-9 expression through NF-kappaB and AP-1 transcription factors by a mechanism quite different than that seen for estrogen-ER.","abstract_html":"In addition to pro-inflammatory agents, the synthetic anti-inflammatory glucocorticoid, dexamethasone, induced PI-9 gene expression via an imperfect glucocorticoid response element (GRE) located at -208. Dexamethasone induced PI-9 mRNA and protein. Dexamethasone-glucocorticoid receptor (GR) complex inhibited IL-1beta induced PI-9 gene expression but IL-1beta did not interfere with dexamethasone induction of PI-9. Glucocorticoid administration resulted in reduced p65 binding to a consensus NF-kappaB element. To investigate the mechanism of crosstalk between Dex-GR and NF-kappaB, we analyzed the effect of dexamethasone on induction of IkappaB-alpha, the inhibitory heterodimer of p65. Dexamethasone induced IkappaBalpha in HepG2 cells. This may be one of the mechanisms used by Dex-GR to interfere with NF-kappaB activity and block IL-1beta-induced PI-9 gene expression. Our findings show that liganded GR may regulate IL-1beta induction of PI-9 expression through NF-kappaB and AP-1 transcription factors by a mechanism quite different than that seen for estrogen-ER.","abstract_has_math":false,"creators":["Thulasiraman, Padmamalini"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Biochemistry","degree_department":null,"school":null,"contributors":["Shapiro, David J."],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-25T22:27:57Z","date_published":"2015-09-25T22:27:57Z","updated_at":"2026-07-22T22:26:23Z","subjects":["Chemistry, Biochemistry"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI3086200"],"render_values":[{"text":"(MiAaPQ)AAI3086200","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/84794","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["Shapiro, David J."]},{"key":"dc:creator","label":"Author","values":["Thulasiraman, Padmamalini"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-25T22:27:57Z","10000-01-01","2003"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Biochemistry"]},{"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":["Chemistry, Biochemistry"]}]},{"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/2142/84794","(MiAaPQ)AAI3086200"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["In addition to pro-inflammatory agents, the synthetic anti-inflammatory glucocorticoid, dexamethasone, induced PI-9 gene expression via an imperfect glucocorticoid response element (GRE) located at -208. Dexamethasone induced PI-9 mRNA and protein. Dexamethasone-glucocorticoid receptor (GR) complex inhibited IL-1beta induced PI-9 gene expression but IL-1beta did not interfere with dexamethasone induction of PI-9. Glucocorticoid administration resulted in reduced p65 binding to a consensus NF-kappaB element. To investigate the mechanism of crosstalk between Dex-GR and NF-kappaB, we analyzed the effect of dexamethasone on induction of IkappaB-alpha, the inhibitory heterodimer of p65. Dexamethasone induced IkappaBalpha in HepG2 cells. This may be one of the mechanisms used by Dex-GR to interfere with NF-kappaB activity and block IL-1beta-induced PI-9 gene expression. Our findings show that liganded GR may regulate IL-1beta induction of PI-9 expression through NF-kappaB and AP-1 transcription factors by a mechanism quite different than that seen for estrogen-ER.","Made available in DSpace on 2015-09-25T22:27:57Z (GMT). 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Dexamethasone induced PI-9 mRNA and protein. Dexamethasone-glucocorticoid receptor (GR) complex inhibited IL-1beta induced PI-9 gene expression but IL-1beta did not interfere with dexamethasone induction of PI-9. Glucocorticoid administration resulted in reduced p65 binding to a consensus NF-kappaB element. To investigate the mechanism of crosstalk between Dex-GR and NF-kappaB, we analyzed the effect of dexamethasone on induction of IkappaB-alpha, the inhibitory heterodimer of p65. Dexamethasone induced IkappaBalpha in HepG2 cells. This may be one of the mechanisms used by Dex-GR to interfere with NF-kappaB activity and block IL-1beta-induced PI-9 gene expression. Our findings show that liganded GR may regulate IL-1beta induction of PI-9 expression through NF-kappaB and AP-1 transcription factors by a mechanism quite different than that seen for estrogen-ER.","Made available in DSpace on 2015-09-25T22:27:57Z (GMT). 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