摘要
Mitophagy is a selective degradation of mitochondria, which also plays a critical role in hematopoiesis. However, it is unclear what role, if any, this process plays in the pathogenesis of beta-thalassemia. To determine the role of mitophagy in beta-thalassemia, CD34(+) hematopoietic progenitor cells (HPCs) were isolated from peripheral blood of beta-thalassemia patients and healthy controls and differentiated into erythrocytes. We found that the ratio of mitochondrial membrane depolarization was significantly increased, and that mitochondria co-localize with lysosomes at a higher level in beta-thalassemia compared with control. Furthermore, the expression of LC3-II and Nix, as well as degradation of p62, in beta-thalassemia was higher than in the control. In sum, our data suggest that selective mitophagy is enhanced during erythrocyte differentiation in beta-thalassemia.
- 出版日期2017-2
- 单位中山大学