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. Author manuscript; available in PMC: 2023 Jul 4.
Published in final edited form as: Sci Transl Med. 2022 Aug 31;14(660):eabj7465. doi: 10.1126/scitranslmed.abj7465

Fig. 2. Neutrophil activation through loss of KLF2 worsens arterial and venous thrombosis.

Fig. 2.

(A) Time to occlusive thrombosis was measured in the carotid artery injury model comparing LysM (n = 7) and K2KO (n = 8) mice. (B) IVC thrombus weight measured after IVC ligation comparing LysM and K2KO mice. n = 8 mice. (C) The timeline shows the experimental model of neutrophil depletion studies in K2KO mice. (D and E) Neutrophils were depleted with anti-Ly6G antibody or control antibody in LysM (n = 6 to 7) and K2KO (n = 6 to 8) mice before (D) arterial or (E) venous thrombosis induction. (F) The timeline depicts adoptive transfer experiments wherein neutrophils were isolated from healthy LysM or K2KO mice and infused into LysM/K2KO mice before arterial or venous thrombosis. (G and H) Infusion of LysM (CRE) or K2KO (KO) neutrophils into respective genotypes (n = 6 to 8 per group) was followed by initiation of (G) arterial and (H) venous thrombosis. Data were analyzed using an unpaired, two-tailed Student’s t test.