| First Author | Renella R | Year | 2014 |
| Journal | Am J Hematol | Volume | 89 |
| Issue | 10 | Pages | 974-7 |
| PubMed ID | 25043722 | Mgi Jnum | J:213707 |
| Mgi Id | MGI:5585658 | Doi | 10.1002/ajh.23796 |
| Citation | Renella R, et al. (2014) Genetic deletion of the GATA1-regulated protein alpha-synuclein reduces oxidative stress and nitric oxide synthase levels in mature erythrocytes. Am J Hematol 89(10):974-7 |
| abstractText | alpha-Synuclein is highly expressed in neural tissue and during erythropoiesis, where the key erythroid regulator GATA1 has been found to modulate its expression. While specific alpha-synuclein (SNCA) mutations are known to cause autosomal dominant familial Parkinson's disease, its wild-type function remains under debate. To investigate the role of alpha-synuclein in murine hematopoiesis and erythropoiesis, we utilized Snca knock-out mice and analyzed erythroid compartments for maturation defects, in vivo erythrocyte survival, and erythrocyte-based reactive oxygen species (ROS) and nitric oxide synthase (NOS) levels. Our findings show that while bone marrow and spleen erythropoiesis and peripheral blood erythrocyte survival in Snca(-/-) mice was comparable to controls, the levels of ROS and of NOS-2 were significantly decreased in mature erythrocytes in these animals. These results indicate a role for alpha-synuclein in regulating oxidative stress in erythrocytes in vivo and could open new avenues for the investigation of its function in non-neural tissue. Am. J. Hematol. 89:974-977, 2014. (c) 2014 Wiley Periodicals, Inc. |
