| First Author | Lin B | Year | 2003 |
| Journal | Acta Pharmacol Sin | Volume | 24 |
| Issue | 12 | Pages | 1199-204 |
| PubMed ID | 14653944 | Mgi Jnum | J:134100 |
| Mgi Id | MGI:3785007 | Citation | Lin B, et al. (2003) CMV-hFasL transgenic mice are sensitive to low doses of streptozotocin-induced type I diabetes mellitus. Acta Pharmacol Sin 24(12):1199-204 |
| abstractText | AIM: To investigate the role of Fas-FasL pathway in the pathogenesis of streptozotocin (STZ)-induced type I diabetes mellitus. METHODS: Low dose injections of STZ were used to induce type I diabetes mellitus in the CMV-hFasL transgenic mice. Blood glucose concentration was measured with Glucotrand Plus blood glucose test strips. Expression of hFasL was detected by RT-PCR and Western blotting. The severity of insulitis was determined by histological examination. Expressions of IL-1beta and TNF-alpha mRNA in the pancreas were detected by semi-quantitative RT-PCR analysis. Fas expression in apoptotic RIN-5F cells was also confirmed by RT-PCR in vitro. RESULTS: hFasL was expressed in the islets of CMV-hFasL transgenic mice. The transgenic mice were sensitive to diabetic induction than the control WT mice. IL-1beta and TNF-alpha expressions in the pancreas of CMV-hFasL transgenic mice were far more than that in WT mice. We also found STZ and IL-1beta could both induce higher expression of Fas in RIN-5F. The combining of Fas-FasL could lead to the apoptosis of beta cells in the CMV-hFasL transgenic mice. CONCLUSION: Fas-FasL interaction plays a significant role in the pathogenic mechanism of type I diabetes mellitus. |
