Journal
ANTIOXIDANTS & REDOX SIGNALING
Volume 9, Issue 7, Pages 855-863Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2007.1568
Keywords
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Funding
- NHLBI NIH HHS [HL55601, HL34300] Funding Source: Medline
- NIDDK NIH HHS [DK068134] Funding Source: Medline
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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 CoPP-treated 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.
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