Figure 2
Figure 2. PF4 drives VSMC proinflammatory response in vivo. (A) The left common carotid artery of WT and PF4−/− mice were ligated, or a sham surgery performed, and plasma PF4 was measured (n = 5 ± SD; *P < .01 vs sham). (B) PF4 is present in the vessel wall on day 9. Immunohistochemistry studies of ligated carotid arteries on days 1 and 9 (representative images). (C) Plasma IL-6 and (D) plasma KC are increased after ligation in WT mice, but not PF4−/− mice, in a similar pattern to PF4 (n = 5 ± SD; *P < .01 vs sham). (E) Ligation-induced IL-6 is primarily vessel wall derived. WT mice were given WT or IL-6−/− bone marrow, and carotid ligations were performed. Postsurgical IL-6 is similar in WT and IL-6−/− bone marrow mice (n = 6 ± SD; *P < .05 vs WT).

PF4 drives VSMC proinflammatory response in vivo. (A) The left common carotid artery of WT and PF4−/− mice were ligated, or a sham surgery performed, and plasma PF4 was measured (n = 5 ± SD; *P < .01 vs sham). (B) PF4 is present in the vessel wall on day 9. Immunohistochemistry studies of ligated carotid arteries on days 1 and 9 (representative images). (C) Plasma IL-6 and (D) plasma KC are increased after ligation in WT mice, but not PF4−/− mice, in a similar pattern to PF4 (n = 5 ± SD; *P < .01 vs sham). (E) Ligation-induced IL-6 is primarily vessel wall derived. WT mice were given WT or IL-6−/− bone marrow, and carotid ligations were performed. Postsurgical IL-6 is similar in WT and IL-6−/− bone marrow mice (n = 6 ± SD; *P < .05 vs WT).

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