| First Author | Fred RG | Year | 2015 |
| Journal | Mol Cell Endocrinol | Volume | 414 |
| Pages | 53-63 | PubMed ID | 26213325 |
| Mgi Jnum | J:228831 | Mgi Id | MGI:5749339 |
| Doi | 10.1016/j.mce.2015.07.015 | Citation | Fred RG, et al. (2015) Role of the AMP kinase in cytokine-induced human EndoC-betaH1 cell death. Mol Cell Endocrinol 414:53-63 |
| abstractText | The aim of the present investigation was to delineate cytokine-induced signaling and death using the EndoC-betaH1 cells as a model for primary human beta-cells. The cytokines IL-1beta and IFN-gamma induced a rapid and transient activation of NF-kappaB, STAT-1, ERK, JNK and eIF-2alpha signaling. The EndoC-betaH1 cells died rapidly when exposed to IL-1beta + IFN-gamma, and this occurred also in the presence of the actinomycin D. Inhibition of NF-kappaB and STAT-1 did not protect against cell death, nor did the cytokines activate iNOS expression. Instead, cytokines promoted a rapid decrease in EndoC-betaH1 cell respiration and ATP levels, and we observed protection by the AMPK activator AICAR against cytokine-induced cell death. It is concluded that EndoC-betaH1 cell death can be prevented by AMPK activation, which suggests a role for ATP depletion in cytokine-induced human beta-cell death. |
