Fig. 1

Myosin1f affects ischemic brain injury through circulating neutrophils. A Myosin1f KO mice has smaller infarction. (a) The experimental procedure. The WT mice are indicated in blue; myosin1f KO mice are indicated in red. (b) Representative TTC-stained brain infarction and quantification of infarct size, which are expressed as percentages to the ischemic hemisphere (p = 0.023). (c) Neurological scores measured 3d after stroke (p = 0.0111, n = 8 mice/group). B Circulating leukocytes are critical for the protective effects of myosin1f^−/− against stroke. (a) Experimental procedures to study the effect of bone marrow transfer on stroke outcomes: after irradiation, recipient WT mice (CD45.2⁻, myosin1f^+/+) received bone marrow cells from WT mice (CD45.2⁺, myosin1f^+/+) or myosin1f^−/− mice (CD45.2⁺, myosin1f^−/−), respectively. Eight weeks later, animals were subjected to MCAO; the infarction and neurological scores were assessed at 3 days after stroke. (b) Infarct sizes: representative TTC staining and quantification of infarctions (p = 0.0263). (c) Neurological score. (p = 0.0353, n = 5 mice/group). C The effects of circulating neutrophil depletion. (a) Experimental procedures: Ly6G antibodies were IV injected 1 day before and 1 day after stroke to deplete neutrophils. (b) Infarct sizes. N = 5 mice/group. (c) Neurological scores. D Adoptive transfer of myosin1f^−/− neutrophils attenuated brain infarction. (a) Experimental procedures to study the effects of neutrophil transfer on stroke outcomes: the recipient mice were IV injected with Ly6G antibodies for neutrophil depletion. The animals then received adoptive transfer of purified neutrophils from WT and myosin1f^−/− mice. Animals were euthanized 2 days later. (b) Infarct sizes (p = 0.0409, n = 5 mice/group). (c) Neurological scores (p = 0.0400, n = 5 mice/group)