MMP-9 was higher at the time of acute MI versus quiescent phase follow-up in acute MI (412 vs. 213 pg/mL, p = 0.001) and atherothrombotic MI specifically (458 vs. 212 pg/mL, p = 0.001).
Specifically, among SCD cases, increased MYL3, VEGFA and MMP9 values in the anterior wall of the right ventricle were found when the confirmed cause of death was acute myocardial infarction (AMI).
The expression of myocardial MMP2 and MMP9 was significantly increased in the AMI group compared with the sham group, whereas that of myocardial netrin-1, TIMP2 and the DCC receptor, was significantly reduced.
The mRNA expressions of MMP-2 and MMP-9 in AMI-CI group were also significantly higher than those in the AMI group, and the differences between the two groups were statistically significant (p<0.05).
Hydroxyproline, COL1A1, miR-26a, p-AKT, and MMP-9 overexpressed, while PTEN downregulated in myocardial tissue during the process of myocardial fibrosis after AMI.
This study demonstrated that CLMN decoction might regulate the expressions of Ccl6, Ccr5, Itgam, Ncf1 and Mmp9, inhibit the chemokine signaling pathway and leukocyte transendothelial migration to play a protective effect on AMI.
Intramyocardial AM administration exacerbated macrophage infiltration, inflammation, and matrix metalloproteinase 9 mRNA expression in the infarct and border zones, whereas disturbed fibrotic repair, then provoked acute cardiac rupture in MI.
Furthermore, HSYA increased the mRNA expressions of VEGF-A and MMP-9 in the extract of antinucleolin antibody-precipitated protein from the heart of AMI mice.
In addition, it suppressed matrix metallopeptidase‑9, transforming growth factor‑β, p38 mitogen‑activated protein kinases (MAPK) and nuclear factor (NF)‑κB protein expression, and promoted B‑cell lymphoma 2 (Bcl‑2) protein expression in AMI mice.
Therefore, our results suggest that TAPE may regulate EPC mobilization through up-regulating the expression level of VEGF, eNOS, NO and MMP-9 in the myocardium of AMI rats.
We determined MMP-9 serum activity by zymography and tissue inhibitor of matrix metalloproteinases (TIMP-1) expression by Western blot and correlated it to RAGE/sRAGE data in patients with cardiogenic shock after acute myocardial infarction (CS, n = 30), in patients with acute myocardial infarction without shock (AMI, n = 20) and in healthy volunteers (n = 20).MMP-9 activity is increased in AMI (P = 0.02 versus controls), but significantly decreased in CS with lowest levels in non-survivors (n = 13, P = 0.02 versus AMI).
We found that MMP9 expression by PBMCs at both the mRNA and protein levels was increased 2-fold (both P<0.05) in patients with acute MI compared with the two control groups.
At a median of 15 weeks after initial clinical presentation, higher circulating levels of MMP2 and MMP9 were independently associated with acute MI after statistical adjustment for conventional risk factors, hs-CRP levels, and cardiac medications.