The aim of this study is to identify gene expression profiles associated with
hyaluronic acid (HA) treatment of normal and osteoarthritis (OA)-like tissue-
engineered cartilage. 3D cartilage micromasses were treated with tumour
necrosis factor-α (TNF-α) (OA-inducer) and/or HA for 7 days. Viability was
examined by PI/FDA staining. To document extracellular matrix (ECM) formation,
glycosaminoglycans (GAG) were stained with Safranin-O and cartilage-specific
type II collagen was detected immunohistochemically. Genome-wide gene
expression was determined using microarray analysis. Normal and OA-like
micromasses remained vital and showed a spherical morphology and homogenous
cell distribution regardless of the treatment. There was no distinct
difference in immunolabeling for type II collagen. Safranin-O staining
demonstrated a typical depletion of GAG in TNF-α-treated micromasses (−73%),
although the extent was limited in the presence of HA (−39%). The microarray
data showed that HA can influence the cartilage metabolism via upregulation of
TIMP3 in OA-like condition. The upregulation of VEGFA and ANKRD37 genes
implies a supportive role of HA in cartilage maturation and survival. The
results of this study validate the feasibility of the in vitro OA model for
the investigation of HA. On the cellular level, no inhibiting or activating
effect of HA was shown. Microarray data demonstrated a minor impact of HA on
gene expression level