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Brief Report

Long-Lasting Expression of HO-1 Delays Progression of Type I Diabetes in NOD Mice

Ming Li, Stephen Peterson, Daniel Husney, Muneo Inaba, Kequan Guo, Attallah Kappas, Susumu Ikehara and Nader G. Abraham

volume 6 | issue 5

1 March 2007
Pages: 567 - 571

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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.

Authors

Ming Li

Kansai Medical University, Moriguchi, Osaka, Japan

Stephen Peterson

New York Medical College, Valhalla, NY

Daniel Husney

New York Medical College, Valhalla, NY

Muneo Inaba

Kansai Medical University, Moriguchi, Osaka, Japan

Kequan Guo

Kansai Medical University, Moriguchi, Osaka, Japan

Attallah Kappas

New York Medical College, Valhalla, NY

Susumu Ikehara

Kansai Medical University, Moriguchi, Osaka, Japan

Nader G. Abraham

New York Medical College, Valhalla, NY



We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
 Download PDF

If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.