Fig. 2

DEX inhibits expression and release of IL-1α by HCAECs in response to inflammatory stimuli. HCAECs were stimulated with 100 ng/ml of TNF-α, or 10 ng/ml of IL-1α or IL-1β, for 48 h in the presence and absence of 10 mg/ml IgG and 1000 nM DEX, alone or in combination. Protein concentrations of IL-1α in HCAEC culture supernatants (a) and mRNA levels of IL-1α in HCAECs (b) were measured by ELISA and qPCR, respectively. Whole-cell lysates of HCAECs were subjected to WB analysis of the expression of IL-1α and heat shock protein 90 (HSP90; as a loading control) (c). Data shown in a and b are the mean ± SD of triplicate samples. All data are representative of two individual experiments using HCAEC lots from different donors. **P < 0.01 compared with 100 ng/ml TNF-α; ††P < 0.01 compared with 10 ng/ml IL-1α; and ‡‡P < 0.01 compared with 10 ng/ml IL-1β