Acute White Matter Injury After Experimental Subarachnoid Hemorrhage: Potential Role of Lipocalin 2

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Abstract

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.

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