| First Author | Egashira Y | Year | 2014 |
| Journal | Stroke | Volume | 45 |
| Issue | 7 | Pages | 2141-3 |
| PubMed ID | 24893611 | Mgi Jnum | J:329501 |
| Mgi Id | MGI:6882292 | Doi | 10.1161/STROKEAHA.114.005307 |
| Citation | Egashira Y, et al. (2014) Acute white matter injury after experimental subarachnoid hemorrhage: potential role of lipocalin 2. Stroke 45(7):2141-3 |
| abstractText | BACKGROUND AND PURPOSE: White matter injury occurs after subarachnoid hemorrhage (SAH) and has not been well studied. In this study, we investigated acute white matter injury in a mouse SAH model and the role of lipocalin 2 (LCN2) in that injury. METHODS: SAH was induced by endovascular perforation in wild-type (WT) or LCN2 knockout (LCN2-/-) mice. Sham WT mice underwent the same procedure without perforation. MRI was performed 24 hours after SAH and the volumes of the T2-hyperintensity in white matter were measured. Immunohistochemistry was performed to determine white matter injury. RESULTS: Mortality rates and SAH severity were not significantly different between WT and LCN2-/- animals. T2-hyperintensity in the white matter was observed in all WT animals at 24 hours after SAH (6.1+/-2.7 versus 0.06+/-0.07 mm3 in sham; P<0.001), and the volume of T2-hyperintensity tended to correlate with SAH severity (r=0.30; P=0.055). In WT animals with SAH, numerous LCN2-positive cells were observed in white matter. In contrast, LCN2-/- animals scarcely developed white matter T2-hyperintensity after SAH (0.5+/-0.5 mm3; P<0.001, versus WT). Markers of axonal damage and myelin degradation were increased in white matter after SAH in WT compared with those in LCN2-/- animals (P<0.05). CONCLUSIONS: SAH results in an acute white matter injury at 24 hours in mice, and LCN2 plays an important role in SAH-induced white matter injury. |
