| First Author | Fidler TP | Year | 2017 |
| Journal | Thromb Haemost | Volume | 117 |
| Issue | 10 | Pages | 1859-1867 |
| PubMed ID | 28771279 | Mgi Jnum | J:339859 |
| Mgi Id | MGI:7524471 | Doi | 10.1160/TH17-03-0174 |
| Citation | Fidler TP, et al. (2017) Superoxide Dismutase 2 is dispensable for platelet function. Thromb Haemost 117(10):1859-1867 |
| abstractText | Increased intracellular reactive oxygen species (ROS) promote platelet activation. The sources of platelet-derived ROS are diverse and whether or not mitochondrial derived ROS, modulates platelet function is incompletely understood. Studies of platelets from patients with sickle cell disease, and diabetes suggest a correlation between mitochondrial ROS and platelet dysfunction. Therefore, we generated mice with a platelet specific knockout of superoxide dismutase 2 (SOD2-KO) to determine if increased mitochondrial ROS increases platelet activation. SOD2-KO platelets demonstrated decreased SOD2 activity and increased mitochondrial ROS, however total platelet ROS was unchanged. Mitochondrial function and content were maintained in non-stimulated platelets. However SOD2-KO platelets demonstrated decreased mitochondrial function following thrombin stimulation. In vitro platelet activation and spreading was normal and in vivo, deletion of SOD2 did not change tail-bleeding or arterial thrombosis indices. In pathophysiological models mediated by platelet-dependent immune mechanisms such as sepsis and autoimmune inflammatory arthritis, SOD2-KO mice were phenotypically identical to wildtype controls. These data demonstrate that increased mitochondrial ROS does not result in platelet dysfunction. |
