| First Author | Oishi K | Year | 2005 |
| Journal | FEBS Lett | Volume | 579 |
| Issue | 17 | Pages | 3555-9 |
| PubMed ID | 15950223 | Mgi Jnum | J:99783 |
| Mgi Id | MGI:3583835 | Doi | 10.1016/j.febslet.2005.05.027 |
| Citation | Oishi K, et al. (2005) Involvement of circadian clock gene Clock in diabetes-induced circadian augmentation of plasminogen activator inhibitor-1 (PAI-1) expression in the mouse heart. FEBS Lett 579(17):3555-9 |
| abstractText | Diabetes is associated with an excess risk of cardiac events, and one of the risk factors for infarction is the elevated-levels of plasminogen activator inhibitor-1 (PAI-1). To evaluate how the molecular clock mechanism is involved in the diabetes-induced circadian augmentation of PAI-1 gene expression, we examined the expression profiles of PAI-1 mRNA in the hearts of Clock mutant mice with streptozotocin-induced diabetes. Circadian expression of PAI-1 mRNA was blunted to low levels under both normal and diabetic conditions in Clock mutant mice, although the expression rhythm was augmented in diabetic wild-type (WT) mice. Furthermore, plasma PAI-1 levels became significantly higher in WT mice than in Clock mutant mice after STZ administration. Our results suggested that the circadian clock component, CLOCK, is involved in the diabetes-induced circadian augmentation of PAI-1 expression in the mouse heart. |
