Interdiction of the diabetic state in NOD mice by sustained induction of heme oxygenase: possible role of carbon monoxide and bilirubin.

Interdiction of the diabetic state in NOD mice by sustained induction of heme oxygenase: possible role of carbon monoxide and bilirubin. Research Abstract Details 

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Interdiction of the diabetic state in NOD mice by sustained induction of heme oxygenase: possible role of carbon monoxide and bilirubin. Abstract Text:

Ming Li,Stephen Peterson,Daniel Husney,Muneo Inaba,Kequan Guo,Eri Terada,Toshisuke Morita,Kiran Patil,Attallah Kappas,Susumu Ikehara,Nader G Abraham,

The aims of the present study were to assess whether sustained HO-1 expression could moderate or prevent diabetes in an animal model of the disease and, if so, to examine the possible mechanisms involved. Our results showed that HO-1 expression and HO activity were upregulated in the pancreas of non-obese diabetic (NOD) mice by the weekly administration of cobalt protoporphyrin (CoPP). Blood glucose levels in CoPPtreated mice decreased to normal, but continuously increased in untreated controls. Beta-cell numbers were preserved in the islets of CoPP-treated mice, whereas no beta cells were found in untreated diabetic mice. The number of CD11c(+) dendritic cells was significantly decreased in the pancreas of CoPP-treated NOD mice, but this effect was reversed by the inhibition of HO activity. Increased levels of HO-1 produced a new pancreatic phenotype, as reflected by increases in phosphorylated AKT, BcL-xL and RSK levels, and decreases in O(2)- and 3-NT levels. These novel findings provide a link between the increase in HO-1 activity, with its concurrent enhanced production of carbon monoxide (CO) and bilirubin, a decrease in infiltrated CD11c(+) dendritic cells and an increase in anti-apoptotic proteins, including RSK and BcL-xL, in the interdiction of the diabetic state.

Interdiction of the diabetic state in NOD mice by sustained induction of heme oxygenase: possible role of carbon monoxide and bilirubin. Publishing Authors By Initials

M Li,S Peterson,D Husney,M Inaba,K Guo,E Terada,T Morita,K Patil,A Kappas,S Ikehara,NG Abraham,

For similar peptides: intracellular signaling peptides and proteins: apoptosis regulatory proteins: proto-oncogene proteins c-bcl-2: bcl-x protein research abstracts see: peptides: intracellular signaling peptides and proteins: apoptosis regulatory proteins: proto-oncogene proteins c-bcl-2: bcl-x protein research

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Interdiction of the diabetic state in NOD mice by sustained induction of heme oxygenase: possible role of carbon monoxide and bilirubin. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Antioxidants & redox signaling

VOLUME: 9

Page Numbers: 855-63

Journal Abbreviation: Antioxid. Redox Signal.

ISSN: 1523-0864

DAY: 3

MONTH: Jul

YEAR: 2007

Interdiction of the diabetic state in NOD mice by sustained induction of heme oxygenase: possible role of carbon monoxide and bilirubin. Information

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LANGUAGE: eng

NlmUniqueID: 100888899

Interdiction of the diabetic state in NOD mice by sustained induction of heme oxygenase: possible role of carbon monoxide and bilirubin. Keywords Mesh Terms:

KEYWORDS: bcl-X Protein

MESH TERMS: metabolism

Chemical & Substance for Abstract: Interdiction of the diabetic state in NOD mice by sustained induction of heme oxygenase: possible role of carbon monoxide and bilirubin. Information

Substance Name: Proto-Oncogene Proteins c-akt

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Interdiction of the diabetic state in NOD mice by sustained induction of heme oxygenase: possible role of carbon monoxide and bilirubin.

AFFILIATION: Department of Pharmacology, New York Medical College, Valhalla, NY 10595, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL55601

ACRONYM: HL

MEDLINETA: Antioxid Redox Signal

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