Document Detail

Glucose deprivation induces heme oxygenase-1 gene expression by a pathway independent of the unfolded protein response.
MedLine Citation:
PMID:  11707454     Owner:  NLM     Status:  MEDLINE    
Nutrients such as glucose regulate the expression of genes that are involved in plasma membrane transport, metabolic functions, and protein trafficking in the endoplasmic reticulum. Depletion of nutrients results in cellular stress, which evokes adaptive and protective responses, one of which is the induction of heme oxygenase-1 (HO-1), a 32-kDa endoplasmic reticulum enzyme that catalyzes the rate-limiting step in heme degradation. Incubation of HepG2 human hepatoma cells in glucose-free medium resulted in an increased HO-1 mRNA content, reaching a maximum of approximately 25-fold over control cells after 12 h. The glucose-dependent induction of HO-1 mRNA was concentration-dependent (k(12) approximately 0.5 mm) and was attenuated by fructose, galactose, mannose, and 2-deoxyglucose, but not by the non-metabolizable glucose analog, 3-O-methylglucose. Tunicamycin, thapsigargin, or azetidine 2-carboxylate, each of which activates the unfolded protein response pathway, did not induce HO-1 mRNA expression, whereas glucose-regulated protein 78 mRNA was increased. These results demonstrate that glucose availability regulates transcription of the HO-1 gene via a pathway that is different from the unfolded protein response. The induction of HO-1 may serve as a protective response in hypoglycemic circumstances and underscores the importance of understanding nutrient control of the HO-1 gene.
Se-Ho Chang; Ione Barbosa-Tessmann; Chin Chen; Michael S Kilberg; Anupam Agarwal
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.     Date:  2001-11-13
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  277     ISSN:  0021-9258     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2002 Jan 
Date Detail:
Created Date:  2002-01-14     Completed Date:  2002-02-13     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1933-40     Citation Subset:  IM    
Department of Medicine, Division of Nephrology, Hypertension & Transplantation and Department of Biochemistry and Molecular Biology, University of Florida, Gainesville, Florida 32610, USA.
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MeSH Terms
Citric Acid Cycle
Gene Expression Regulation, Enzymologic*
Glucose / metabolism*
Heme Oxygenase (Decyclizing) / biosynthesis,  chemistry,  genetics*
Protein Denaturation
RNA, Messenger / genetics
Tumor Cells, Cultured
Grant Support
Reg. No./Substance:
0/RNA, Messenger; 50-99-7/Glucose; EC Oxygenase (Decyclizing)

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