Open AccessDiabetes influences cardiac extracellular matrix remodelling after myocardial infarction and subsequent development of cardiac dysfunction
Author(s) -
Eguchi Megumi,
Xu Guoxiong,
Li RenKe,
Sweeney Gary
Publication year - 2012
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/j.1582-4934.2012.01613.x
Subject(s) - cardiology , medicine , myocardial infarction , diabetes mellitus , ejection fraction , cardiac function curve , diabetic cardiomyopathy , masson's trichrome stain , streptozotocin , extracellular matrix , stroke volume , ventricular remodeling , infarction , endocrinology , fibrosis , heart failure , biology , cardiomyopathy , microbiology and biotechnology
This study was conducted to examine the influence of acute streptozotocin‐induced diabetes on cardiac remodelling and function in mice subjected to myocardial infarction ( MI ) by coronary artery ligation. Echocardiography analysis indicated that diabetes induced deleterious cardiac functional changes as demonstrated by the negative differences of ejection fraction, fractional shortening, stroke volume, cardiac output and left ventricular volume 24 hrs after MI . Temporal analysis for up to 2 weeks after MI showed higher mortality in diabetic animals because of cardiac wall rupture. To examine extracellular matrix remodelling, we used fluorescent molecular tomography to conduct temporal studies and observed that total matrix metalloproteinase ( MMP ) activity in hearts was higher in diabetic animals at 7 and 14 days after MI , which correlated well with the degree of collagen deposition in the infarct area visualized by scanning electron microscopy. Gene arrays indicated temporal changes in expression of distinct MMP isoforms after 1 or 2 weeks after MI , particularly in diabetic mice. Temporal changes in cardiac performance were observed, with a trend of exaggerated dysfunction in diabetic mice up to 14 days after MI . Decreased radial and longitudinal systolic and diastolic strain rates were observed over 14 days after MI , and there was a trend towards altered strain rates in diabetic mouse hearts with dyssynchronous wall motion clearly evident. This correlated with increased collagen deposition in remote areas of these infarcted hearts indicated by Masson's trichrome staining. In summary, temporal changes in extracellular matrix remodelling correlated with exaggerated cardiac dysfunction in diabetic mice after MI .