PLT-derived FasL contributes to tissue apoptosis in vivo. (A-E) PF4-Cre⁺ FasL^fl/fl mice were generated and stroke was induced by tMCAO. PF4-Cre⁻ FasL^fl/fl mice served as control. (A-B) We observed no difference in peripheral PLT counts and bleeding time between Cre⁻ littermates and PF4-Cre⁺ FasL^fl/fl mice. (C-D) Apoptosis was quantified in brain sections using TUNEL staining. Neuronal apoptosis is presented as the percentage of TUNEL positive cells (red) of total cell number per section. Nuclei were stained using DAPI (blue). Data are mean ± SEM (n = 6, 5 non-consecutive sections per animal were analyzed). *P < .05 vs control animals. (C) Depicts representative images of the analyzed sections. (E) PF4-Cre⁺ FasL^fl/fl mice were injected with control liposomes or clodronate liposomes to deplete macrophages before stroke induction, and apoptosis was assessed within the brain tissue by TUNEL staining. Furthermore, PF4-Cre⁻ FasL^fl/fl mice were used as control. Data are mean ± SEM (n = 6, 3 non-consecutive sections per animal were analyzed). *P < .05 for PF4-Cre⁺ animals treated with clodronate liposomes or control liposomes in comparison with PF4-Cre⁻ control animals. n.s., no significance.