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MMP‐9 dependent proteins regulate left ventricular remodeling following myocardial infarction
Author(s) -
Castro Bras Lisandra Eunice,
DeLeon Kristine Y.,
Yabluchanskiy Andriy,
Ma Yonggang,
Halade Ganesh V.,
Hakala Kevin,
Weintraub Susan T.,
Lindsey Merry L.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1129.4
Subject(s) - periostin , extracellular matrix , ventricular remodeling , matrix metalloproteinase , fibronectin , myocardial infarction , ventricle , ejection fraction , chemistry , heart failure , medicine , cardiology , microbiology and biotechnology , biology , biochemistry
Adverse remodeling of the left ventricle (LV) following myocardial infarction (MI) is a leading cause of congestive heart failure. Extracellular matrix (ECM) turnover is a key component of LV remodeling that involves the degradation of ECM to remove dead myocytes as well as synthesis of new ECM to form the infarct scar. Post‐MI, matrix metalloproteinase (MMP)‐9 is a prognostic indicator of LV dysfunction. Identification and quantification of ECM proteins are hampered by the low solubility of ECM components in standard tissue preparation reagents. We developed a novel differential solubility‐based‐method for protein fractionation optimized for the analysis of cardiac ECM. We used this novel method coupled with a proteomic approach to evaluate the LV infarct regions of wild type (WT; n=8) and MMP‐9 null (null; n=8) mice at 5 days post‐MI. Our method generated 3 protein fractions per sample: soluble, cytoplasmic and insoluble. By HPLC‐ESI‐MS/MS analysis of the insoluble fraction, we identified 157 proteins, of which 22 (14%) were ECM proteins. Fibronectin increased post‐MI in both genotypes (number of assigned spectra: 2 to 55 in WT vs 4 to 87 in null). Periostin was only observed post‐MI (number of assigned spectra: 6 WT vs 20 null). In conclusion, fibronectin and periostin may mediate LV remodeling through MMP‐9 dependent mechanisms.