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. Author manuscript; available in PMC: 2016 Apr 15.
Published in final edited form as: Int J Cardiol. 2015 Mar 5;185:198–208. doi: 10.1016/j.ijcard.2015.03.054

Figure 6. MMP-12 inhibition resulted in higher hyaluronic acid (HA) levels at d1, prolonged accumulation at d7, and reduced apoptosis at d7 post-MI.

Figure 6

(A) The CD44 ligand, HA, was elevated at d1 post-MI in the MMP-12 inhibitor (MMP-12i) group compared to the saline group, and these levels were sustained through d7 post-MI. n=6/group. *p<0.05 vs. day 0, #p<0.05 vs. respective saline. (B) MMP-12i increased protein expression of caspase 3, an apoptosis marker. Peritoneal macrophages were used as a positive control (labeled as C). (C) Immunohistochemistry analysis showed that cleaved caspase 3 expression was reduced in the infarct area of MMP-12i group at d7 post-MI compared to the saline MI group. (D) CD18, an adhesion molecule that suppresses apoptosis, was upregulated in the MMP-12i group compared to saline at d7 post-MI. Peritoneal macrophages were used as a positive control (labeled as C). n=5–10/ group, *p<0.05 vs. day 0 and #p<0.05 vs. d7 saline. Scale bar is 200 μm.