Hyaluronan, a ubiquitous high-molecular-mass glycinoglycan on cell
surfaces and in extracellular matrices, has a number of specific signaling
functions in cell–cell communication. Changes in its content, molecular
mass and turnover rate are crucial for cell proliferation, migration and
apoptosis, processes that control tissue remodeling during embryonic devel-opment, inflammation, injury and cancer.
As observedpreviously in culturedhuman skinfibroblasts, a
decrease of hyaluronan production was also observed in
group C Streptococcus equi FM100 cells treated with
4-methylumbelliferone (MU), although there was no effect
on their growth. In this study, the inhibition mechanism of
hyaluronan synthesis by MU was examined usingStrepto-coccus equiFM100, as a model.
Hyaluronan matrices are ubiquitous in normal and pathological biological
processes. This remarkable diversity is related to their unique mechanism
of synthesis by hyaluronan synthases. These enzymes are normally acti-vated in the plasma membrane and utilize cytosolic substrates directly to
form these large polyanionic glycosaminoglycans, which are extruded
directly into the extracellular space.