Figure 7.
Figure 7. Reversal of the antiproliferative effect of cleaved antithrombin on bFGF-stimulated HUVECs by TGF-β1–induced overexpression of perlecan. HUVECs were cultured with or without 10 μg/mL native (N) or cleaved (C) forms of antithrombin in the absence or presence of 10 ng/mL bFGF and/or 5 ng/mL TGF-β1 as indicated for 48 hours, and then the numbers of viable cells were counted as described in “Materials and methods.” (A) The number of viable cells expressed relative to the control as mean ± SD (bars) from 3 independent determinations. *A statistically significant difference from the control in the absence of TGF-β1 (P < .001). (B) The relative perlecan and β-actin control mRNA levels measured in bFGF-stimulated HUVECs cultured in the absence (lanes 1 to 3) or in the presence of TGF-β1 (lanes 4 to 6) by semiquantitative RT-PCR as in Figure 4.

Reversal of the antiproliferative effect of cleaved antithrombin on bFGF-stimulated HUVECs by TGF-β1–induced overexpression of perlecan. HUVECs were cultured with or without 10 μg/mL native (N) or cleaved (C) forms of antithrombin in the absence or presence of 10 ng/mL bFGF and/or 5 ng/mL TGF-β1 as indicated for 48 hours, and then the numbers of viable cells were counted as described in “Materials and methods.” (A) The number of viable cells expressed relative to the control as mean ± SD (bars) from 3 independent determinations. *A statistically significant difference from the control in the absence of TGF-β1 (P < .001). (B) The relative perlecan and β-actin control mRNA levels measured in bFGF-stimulated HUVECs cultured in the absence (lanes 1 to 3) or in the presence of TGF-β1 (lanes 4 to 6) by semiquantitative RT-PCR as in Figure 4.

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