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National Institute of Environmental Health Sciences

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Publication Detail

Title: Differential Regulation of Bcl-xL Gene Expression by Corticosterone, Progesterone, and Retinoic Acid.

Authors: Morrissy, Steve J; Sun, Haipeng; Zhang, Jack; Strom, Joshua; Chen, Qin M

Published In J Biochem Mol Toxicol, (2016 Jun)

Abstract: Corticosterone (CT), progesterone (PG), and retinoic acid (RA) are capable of inhibiting Doxorubicin (Dox) from inducing apoptosis in rat cardiomyocytes. Mechanistically, CT, PG, and RA induce increases of Bcl-xL protein and mRNA, and activate a 3.2 kb bcl-x gene promoter. CT and RA, but not PG, induced the activity of a 0.9 kb bcl-x promoter, containing sequences for AP-1 and NF-kB binding. RA, but not CT or PG, induced NF-kB activation. CT, but not PG or RA, induced AP-1 activation, and induction of the 0.9 kb bcl-x reporter by CT was inhibited by dominant negative c-Jun TAM-67 or removal of AP-1 binding site. Therefore, although CT, PG, and RA all induce Bcl-xL mRNA and protein, three independent mechanisms are in operation: while CT induces Bcl-xL via AP-1 transcription factor, and RA induces NF-kB activation and bcl-x promoter activity, PG induces Bcl-xL via a mechanism independent of NF-kB or AP-1.

PubMed ID: 26915917 Exiting the NIEHS site

MeSH Terms: Animals; Animals, Newborn; Antibiotics, Antineoplastic/toxicity; Apoptosis/drug effects; Apoptosis/genetics; Binding Sites; Corticosterone/pharmacology*; Doxorubicin/antagonists & inhibitors; Doxorubicin/toxicity; Gene Expression Regulation*; Genes, Reporter; Luciferases/genetics; Luciferases/metabolism; Myocytes, Cardiac/cytology; Myocytes, Cardiac/drug effects*; Myocytes, Cardiac/metabolism; NF-kappa B/genetics; NF-kappa B/metabolism; Peptide Fragments/genetics; Peptide Fragments/metabolism; Primary Cell Culture; Progesterone/pharmacology*; Promoter Regions, Genetic; Protein Binding; Proto-Oncogene Proteins c-jun/genetics; Proto-Oncogene Proteins c-jun/metabolism; RNA, Messenger/genetics*; RNA, Messenger/metabolism; Rats; Signal Transduction; Transcription Factor AP-1/genetics; Transcription Factor AP-1/metabolism; Tretinoin/pharmacology*; bcl-X Protein/genetics*; bcl-X Protein/metabolism

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