Abstract:
AIMS:Cardiovascular disease is the leading cause of death for individuals diagnosed with type II diabetes mellitus (DM). Changes in cardiac function, left ventricular wall thickness and fibrosis have all been described in patients and animal models of diabetes; however, the factors mediating increased matrix deposition remain unclear. The goal of this study was to evaluate whether cardiac fibroblast function is altered in a rat model of type II DM. MAIN METHODS:Cardiac fibroblasts were isolated from 14 week old Zucker diabetic and lean control (LC) adult male rat hearts. Fibroblasts were examined for their ability to remodel 3-dimensional collagen matrices, their adhesion, migration and proliferation on collagen and changes in gene expression associated with collagen remodeling. KEY FINDINGS:Cardiac fibroblasts from diabetic animals demonstrated significantly greater ability to contract 3-dimensional collagen matrices compared to cardiac fibroblasts from LC animals. The enhanced contractile behavior was associated with an increase in diabetic fibroblast proliferation and elevated expression of α-smooth muscle actin and type I collagen, suggesting the transformation of diabetic fibroblasts into a myofibroblast phenotype. SIGNIFICANCE:Cardiac fibrosis is a common complication in diabetic cardiomyopathy which may contribute to the observed cardiac dysfunction associated with this disease. Identifying and understanding the changes in fibroblast behavior which contribute to the increased deposition of collagen and other matrix proteins may provide novel therapeutic targets for reducing the devastating effects of diabetes on the heart.
journal_name
Life Scijournal_title
Life sciencesauthors
Fowlkes V,Clark J,Fix C,Law BA,Morales MO,Qiao X,Ako-Asare K,Goldsmith JG,Carver W,Murray DB,Goldsmith ECdoi
10.1016/j.lfs.2013.01.003subject
Has Abstractpub_date
2013-03-28 00:00:00pages
669-76issue
11eissn
0024-3205issn
1879-0631pii
S0024-3205(13)00004-0journal_volume
92pub_type
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