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. 2017 Mar 28;113(8):892–905. doi: 10.1093/cvr/cvx053

Figure 4.

Figure 4

tTG loss increases myocardial MMP2 activity and is associated with accentuated upregulation of LOXL1, LOXL2 and LOXL4 in the pressure-overloaded myocardium. (A and B) Zymography demonstrated that after 28 days of pressure overload tTG KO animals had increased myocardial MMP2 activity when compared with WT animals (*P < 0.05 vs. WT, n = 6–7/group, unpaired t-test). (C) Increased MMP2 activity in tTG null hearts was not due to increased MMP2 transcription. After 28 days of TAC, MMP2 mRNA levels were comparable between WT and tTG KO hearts (**P < 0.01 vs. corresponding sham, Kruskal–Wallis test, n = 6–12/group). (D–H) tTG absence had significant effects on expression of matrix cross-linking genes in the pressure overloaded myocardium (^P < 0.05, ^^P < 0.01 vs. corresponding shams). In comparison to corresponding WT animals, tTG KO mice had significantly increased LOXL1, LOXL2 and LOXL4 mRNA levels after 3–28 days of TAC (*P < 0.05, **P < 0.01, n = 6–17/group, parametric ANOVA followed by Sidak’s test or Kruskal–Wallis test).