التفاصيل البيبلوغرافية
| العنوان: |
CXCL10 Impairs β Cell Function and Viability in Diabetes through TLR4 Signaling. |
| المؤلفون: |
Schulthess, Fabienne T., Paroni, Federico, Sauter, Nadine S., Shu, Luan, Ribaux, Pascale, Haataja, Leena, Strieter, Robert M., Oberholzer, Jose, King, Charles C., Maedler, Kathrin |
| المصدر: |
Cell Metabolism; Feb2009, Vol. 9 Issue 2, p125-139, 15p |
| مصطلحات موضوعية: |
APOPTOSIS, CELL physiology, TREATMENT of diabetes, ANTIVIRAL agents |
| مستخلص: |
Summary: In type 1 and type 2 diabetes (T1/T2DM), β cell destruction by apoptosis results in decreased β cell mass and progression of the disease. In this study, we found that the interferon γ-inducible protein 10 plays an important role in triggering β cell destruction. Islets isolated from patients with T2DM secreted CXCL10 and contained 33.5-fold more CXCL10 mRNA than islets from control patients. Pancreatic sections from obese nondiabetic individuals and patients with T2DM and T1DM expressed CXCL10 in β cells. Treatment of human islets with CXCL10 decreased β cell viability, impaired insulin secretion, and decreased insulin mRNA. CXCL10 induced sustained activation of Akt, JNK, and cleavage of p21-activated protein kinase 2 (PAK-2), switching Akt signals from proliferation to apoptosis. These effects were not mediated by the commonly known CXCL10 receptor CXCR3 but through TLR4. Our data suggest CXCL10 as a binding partner for TLR4 and as a signal toward β cell failure in diabetes. [Copyright &y& Elsevier] |
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