Proteomic analysis identifies in vivo candidate matrix metalloproteinase-9 substrates in the left ventricle post-myocardial infarction

2010 ◽  
Vol 4 (10-11) ◽  
pp. 849-849
Author(s):  
Rogelio Zamilpa ◽  
Elizabeth F. Lopez ◽  
Ying Ann Chiao ◽  
Qiuxia Dai ◽  
Gladys P. Escobar ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Matrix Metalloproteinase ◽  
Proteomic Analysis ◽  
Matrix Metalloproteinase 9 ◽  
Post Myocardial Infarction ◽  
Metalloproteinase 9

scholarly journals Proteomic analysis identifies in vivo candidate matrix metalloproteinase-9 substrates in the left ventricle post-myocardial infarction

PROTEOMICS ◽  
2010 ◽  
Vol 10 (11) ◽  
pp. 2214-2223 ◽  
Author(s):  
Rogelio Zamilpa ◽  
Elizabeth F. Lopez ◽  
Ying Ann Chiao ◽  
Qiuxia Dai ◽  
Gladys P. Escobar ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Left Ventricle ◽  
Matrix Metalloproteinase ◽  
Proteomic Analysis ◽  
Matrix Metalloproteinase 9 ◽  
Post Myocardial Infarction ◽  
Metalloproteinase 9

scholarly journals P. gingivalis lipopolysaccharide intensifies inflammation post-myocardial infarction through matrix metalloproteinase-9

2014 ◽  
Vol 76 ◽  
pp. 218-226 ◽  
Author(s):  
Kristine Y. DeLeon-Pennell ◽  
Lisandra E. de Castro Brás ◽  
Rugmani Padmanabhan Iyer ◽  
Dustin R. Bratton ◽  
Yu-Fang Jin ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 9 ◽  
Post Myocardial Infarction ◽  
Metalloproteinase 9

scholarly journals Citrate Synthase Is a Novel In Vivo Matrix Metalloproteinase-9 Substrate That Regulates Mitochondrial Function in the Postmyocardial Infarction Left Ventricle

2014 ◽  
Vol 21 (14) ◽  
pp. 1974-1985 ◽  
Author(s):  
Lisandra E. de Castro Brás ◽  
Courtney A. Cates ◽  
Kristine Y. DeLeon-Pennell ◽  
Yonggang Ma ◽  
Rugmani Padmanabhan Iyer ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Matrix Metalloproteinase ◽  
Mitochondrial Function ◽  
Citrate Synthase ◽  
Matrix Metalloproteinase 9 ◽  
Postmyocardial Infarction ◽  
Metalloproteinase 9

Abstract 13389: Early Matrix Metalloproteinase-9 Inhibition Stimulates Neutrophil Infiltration and Delays Neutrophil Apoptosis Post-Myocardial Infarction in Mice

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Rugmani P Iyer ◽  
Nicolle L Patterson ◽  
Gregg B Fields ◽  
Merry L Lindsey
Keyword(s):  
Myocardial Infarction ◽  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 9 ◽  
Post Myocardial Infarction ◽  
Coronary Artery Ligation ◽  
Neutrophil Apoptosis ◽  
Inflammatory Genes ◽  
Apoptotic Markers ◽  
Significant Difference ◽  
Metalloproteinase 9

Matrix metalloproteinase-9 (MMP-9) increases in the first week post-MI, and targeted deletion of the MMP-9 gene attenuates cardiac remodeling post-myocardial infarction (MI), but whether MMP-9 inhibition early post-MI is effective therapeutic strategy has not been evaluated. Adult male C57BL/6J mice (3-6 months old, n=80) were subjected to coronary artery ligation. Saline or MMP-9 inhibitor (MMP-9i; 0.03 μg/day) was delivered at 3 h post-MI, and the mice were sacrificed at days 1 or 7 post-MI. Infarct area was similar in the saline (57±1%) and MMP-9i (55±1%) groups (p=0.22), indicating equal initial injury. The 7 day post-MI survival rates showed no significant difference between saline and MMP-9i groups (p=0.54). MMP-9 inhibition resulted in a 31±1% reduction in MMP-9 activity at day 1 post-MI (p<0.05 vs. saline). Surprisingly, MMP-9 inhibition worsened LV function at day 7 post-MI, as shown by ejection fractions of 13±1% for saline vs. 8±1% for MMP-9i (p<0.05). Of 84 inflammatory genes examined in the day 7 infarct, 15 pro-inflammatory genes were increased and one decreased in the MMP-9i group (all p<0.05 vs. saline). Because MMP-9i showed increased inflammation at day 7, we measured neutrophil numbers. The saline group showed increased neutrophils at day 1, with numbers declining by day 7 due to induction of apoptosis. In MMP-9i, neutrophils were 2-fold higher at day 1 and persisted at day 7 for an 18-fold difference from saline, indicating prolonged neutrophil presence. Isolated blood neutrophils stimulated with active MMP-9 showed increased levels of pro-apoptotic markers Bcl and Bax compared to unstimulated control (both p<0.05). Interestingly, neutrophils stimulated with active MMP-9 and treated with MMP-9i showed increased levels of anti-apoptotic markers Mcl and Xiap (both p<0.05) compared to MMP-9 treated cells. This suggests that prolonged neutrophil presence with the MMP-9 inhibition was due to a dramatic reduction in neutrophil apoptosis. In conclusion, MMP-9 inhibition starting immediately post-MI decreased neutrophil apoptosis leading to increased inflammation and resulting in exacerbated LV dysfunction. Cat: 515 - Apoptosis and Necrosis

scholarly journals Early matrix metalloproteinase-9 inhibition post-myocardial infarction worsens cardiac dysfunction by delaying inflammation resolution

2016 ◽  
Vol 100 ◽  
pp. 109-117 ◽  
Author(s):  
Rugmani Padmanabhan Iyer ◽  
Lisandra E. de Castro Brás ◽  
Nicolle L. Patterson ◽  
Manishabrata Bhowmick ◽  
Elizabeth R. Flynn ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Matrix Metalloproteinase ◽  
Cardiac Dysfunction ◽  
Matrix Metalloproteinase 9 ◽  
Post Myocardial Infarction ◽  
Inflammation Resolution ◽  
Metalloproteinase 9
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