| First Author | Shavit-Stein E | Year | 2021 |
| Journal | PLoS One | Volume | 16 |
| Issue | 3 | Pages | e0248431 |
| PubMed ID | 33720950 | Mgi Jnum | J:304553 |
| Mgi Id | MGI:6513027 | Doi | 10.1371/journal.pone.0248431 |
| Citation | Shavit-Stein E, et al. (2021) Ischemic stroke in PAR1 KO mice: Decreased brain plasmin and thrombin activity along with decreased infarct volume. PLoS One 16(3):e0248431 |
| abstractText | BACKGROUND: Ischemic stroke is a common and debilitating disease with limited treatment options. Protease activated receptor 1 (PAR1) is a fundamental cell signaling mediator in the central nervous system (CNS). It can be activated by many proteases including thrombin and plasmin, with various down-stream effects, following brain ischemia. METHODS: A permanent middle cerebral artery occlusion (PMCAo) model was used in PAR1 KO and WT C57BL/6J male mice. Mice were evaluated for neurological deficits (neurological severity score, NSS), infarct volume (Tetrazolium Chloride, TTC), and for plasmin and thrombin activity in brain slices. RESULTS: Significantly low levels of plasmin and thrombin activities were found in PAR1 KO compared to WT (1.6+/-0.4 vs. 3.2+/-0.6 ng/mul, p<0.05 and 17.2+/-1.0 vs. 21.2+/-1.0 mu/ml, p<0.01, respectively) along with a decreased infarct volume (178.9+/-14.3, 134.4+/-13.3 mm3, p<0.05). CONCLUSIONS: PAR1 KO mice have smaller infarcts, with lower thrombin and plasmin activity levels. These findings may suggest that modulation of PAR1 is a potential target for future pharmacological treatment of ischemic stroke. |
