Growth of SF on LN1-coated surfaces without additional stimuli induced a significant IL-8 mRNA response (3.1-fold, ± 1.24, P ≤ 0.001) and lower responses for IL-1β, IL-16, IL-1α, IL-18 and IL-6. MMP-1 mRNA was upregulated 2.3-fold (± 0.79, P ≤ 0.001), and MMP-3 mRNA only 1.5-fold. Upon incubated of SF on LN10, cytokine and MMP expressions were not changed. Addition of TGF-β (10 ng/ml, 24 hours) to SF attached to tissue culture vessels showed a different induction profile. Here IL-6, IL-1β, IL-1α, IL-8, IL-16 and MMP-1 mRNAs were induced to some degree, IL-18 mRNA was reduced whereas MMP-3 mRNA was induced (3.15-fold, ± 0.7, P ≤ 0.04), when compared with controls. Next combinations of activation by TGF-β and laminin signaling were investigated. For cytokine expressions no additive effects of combining these signals were seen and MMP-1 mRNA was induced to some extent (threefold, ± 1.76). In contrast, MMP-3 mRNA was induced more that 10-fold (12.8 ± 8.7, P ≤ 0.025) and MMP-3 secretion was elevated almost 20-fold (19.67 ± 6.9, P ≤ 0.06). In SF, mRNAs encoding α1, β1 and γ1 laminin – which encode the proteins for LN1 – were detected by quantitative RT-PCR and transcript amounts encoding the α1 and β1 chains of LN1 were higher than mRNA encoding the LN1 γ1 chain. Using an anti-EHS serum, LN1 was detected on SF by immunocytochemistry. However, using monoclonal antibodies to laminin α1 or β1 proteins, staining signals were very weak.