Biglycan, a
small leucine-rich proteoglycan, has been shown to interact with extracellular matrix (ECM)
collagen and may influence fibrillogenesis. We hypothesized that
biglycan contributes to post-
myocardial infarction (MI)
scar development and that the absence of
biglycan would result in altered
scar structure and mechanics. Anterior MI was induced in
biglycan hemizygous null and wild-type mice by permanent
ligation of the left coronary artery. The initial extent of ischemic injury was similar in the two groups, as was the
infarct size after 30 days, although there was some tendency toward reduced expansion in the
biglycan-null. Electron microscopy revealed that
collagen fibrils had a smaller average diameter and a narrower range in the
biglycan-null
scar, as well as appearing more densely packed. In vivo strain analysis showed that
biglycan-null
scars were stiffer than the wild-type. Remote LV
collagen concentration tended to be reduced in
biglycan-null hearts, but the difference was not statistically significant. Null-expression of
biglycan may alter
collagen fibril ultrastructure, and thereby influence
scar mechanics and remodeling.