Document Detail


Inhibition of deoxyhypusine synthase enhances islet {beta} cell function and survival in the setting of endoplasmic reticulum stress and type 2 diabetes.
MedLine Citation:
PMID:  20956533     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Islet β cell dysfunction resulting from inflammation, ER stress, and oxidative stress is a key determinant in the progression from insulin resistance to type 2 diabetes mellitus. It was recently shown that the enzyme deoxyhypusine synthase (DHS) promotes early cytokine-induced inflammation in the β cell. DHS catalyzes the conversion of lysine to hypusine, an amino acid that is unique to the translational elongation factor eIF5A. Here, we sought to determine whether DHS activity contributes to β cell dysfunction in models of type 2 diabetes in mice and β cell lines. A 2-week treatment of obese diabetic C57BLKS/J-db/db mice with the DHS inhibitor GC7 resulted in improved glucose tolerance, increased insulin release, and enhanced β cell mass. Thapsigargin treatment of β cells in vitro induces a picture of ER stress and apoptosis similar to that seen in db/db mice; in this setting, DHS inhibition led to a block in CHOP (CAAT/enhancer binding protein homologous protein) production despite >30-fold activation of Chop gene transcription. Blockage of CHOP translation resulted in reduction of downstream caspase-3 cleavage and near-complete protection of cells from apoptotic death. DHS inhibition appeared to prevent the cytoplasmic co-localization of eIF5A with the ER, possibly precluding the participation of eIF5A in translational elongation at ER-based ribosomes. We conclude that hypusination by DHS is required for the ongoing production of proteins, particularly CHOP, in response to ER stress in the β cell.
Authors:
Reiesha D Robbins; Sarah A Tersey; Takeshi Ogihara; Dhananjay Gupta; Thomas B Farb; James Ficorilli; Krister Bokvist; Bernhard Maier; Raghavendra G Mirmira
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-10-18
Journal Detail:
Title:  The Journal of biological chemistry     Volume:  285     ISSN:  1083-351X     ISO Abbreviation:  J. Biol. Chem.     Publication Date:  2010 Dec 
Date Detail:
Created Date:  2010-12-14     Completed Date:  2011-01-11     Revised Date:  2011-12-19    
Medline Journal Info:
Nlm Unique ID:  2985121R     Medline TA:  J Biol Chem     Country:  United States    
Other Details:
Languages:  eng     Pagination:  39943-52     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, University of Virginia, Charlottesville, Virginia 22904, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis*
Caspase 3 / genetics,  metabolism
Cell Survival / genetics
Diabetes Mellitus, Type 2 / enzymology*,  genetics,  pathology
Endoplasmic Reticulum / genetics,  metabolism*,  pathology
Enzyme Inhibitors / pharmacology
Insulin-Secreting Cells / enzymology*,  pathology
Mice
Mice, Mutant Strains
Oxidoreductases Acting on CH-NH Group Donors / genetics,  metabolism*
Peptide Chain Elongation, Translational / drug effects,  genetics
Peptide Initiation Factors / genetics,  metabolism
RNA-Binding Proteins / genetics,  metabolism
Thapsigargin / pharmacology
Transcription Factor CHOP / biosynthesis,  genetics
Unfolded Protein Response*
Grant Support
ID/Acronym/Agency:
F31 DK079420/DK/NIDDK NIH HHS; R01 DK60581/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Ddit3 protein, mouse; 0/Enzyme Inhibitors; 0/Peptide Initiation Factors; 0/RNA-Binding Proteins; 0/eukaryotic translation initiation factor 5A; 147336-12-7/Transcription Factor CHOP; 67526-95-8/Thapsigargin; EC 1.5.-/Oxidoreductases Acting on CH-NH Group Donors; EC 1.5.1.-/deoxyhypusine synthase; EC 3.4.22.-/Casp3 protein, mouse; EC 3.4.22.-/Caspase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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