Document Detail

Long-lasting expression of HO-1 delays progression of type I diabetes in NOD mice.
MedLine Citation:
PMID:  17299269     Owner:  NLM     Status:  MEDLINE    
Heme oxygenase-1 (HO-1) is crucial in regulating oxidative injury. The present study was designed to assess whether HO-1 upregulation by cobalt protoporphyrin IX (CoPP) moderates or prevents the diabetic state in non-obese diabetic (NOD) mice, an animal model for Type 1 diabetes (T1D). HO-1 expression and HO activity were upregulated in the pancreas by the intermittent administration of CoPP. This was associated with decreases in blood glucose and pancreatic O2-, but increased pAKT and BcL-XL and cell survival. A considerable number of beta cells were preserved in the islets of CoPP-treated NOD mice, while none were found in untreated diabetic mice. The number of CD11c+ dendritic cells was decreased in the pancreas of CoPP-treated NOD mice (p < 0.05). These novel findings provide a link between the increase in HO-1 and a decrease in infiltrated CD11c+ dendritic cells, and suggest that induction of HO-1 activity can be used to enhance cell survival and moderate the diabetic state in T1D.
Ming Li; Stephen Peterson; Daniel Husney; Muneo Inaba; Kequan Guo; Attallah Kappas; Susumu Ikehara; Nader G Abraham
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2007-03-29
Journal Detail:
Title:  Cell cycle (Georgetown, Tex.)     Volume:  6     ISSN:  1551-4005     ISO Abbreviation:  Cell Cycle     Publication Date:  2007 Mar 
Date Detail:
Created Date:  2007-03-19     Completed Date:  2007-05-03     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  101137841     Medline TA:  Cell Cycle     Country:  United States    
Other Details:
Languages:  eng     Pagination:  567-71     Citation Subset:  IM    
First Department of Pathology, Kansai Medical University, Moriguchi, Osaka, Japan.
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MeSH Terms
Blood Glucose / metabolism
Diabetes Mellitus, Type 1 / enzymology*,  pathology,  prevention & control*
Disease Progression
Gene Expression Regulation, Enzymologic / physiology*
Heme Oxygenase-1 / biosynthesis*,  genetics
Mice, Inbred NOD
Pancreas / enzymology,  pathology
Grant Support
Reg. No./Substance:
0/Blood Glucose; EC Oxygenase-1

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