Fig. 7

Fig. 7

FGF-2 leads to the accumulation of sVEGFR1 splice variants in endothelial cells. a Dose effects of FGF-2 in HUVEC and HDMEC treated or not (NT) for 72 h with increasing concentrations of FGF-2. Left panel: representative RT-PCR analyses of VEGFR1 and sVEGFR1-ex15a, sVEGFR1-i13, and sVEGFR1-ex12 splice variants. GAPDH was used as an internal control. Right panel: semi-quantification using ImageJ software of PCR-specific signals related to GAPDH signal in 3nM FGF-2-treated cells. Ratio obtained in nontreated (NT) condition was arbitrarily assigned the value 1 (mean ± SD, unpaired t test, *p<0.05, **p<0.01, ns: not significant). Numbers below the graph indicate the number of biological replicates for each condition. b, c RT-qPCR analyses of VEGFR1 (black bars), sVEGFR1-ex15 (hatched bars), sVEGFR1-i13 (white bars), and sVEGFR1-ex12 (gray bars) mRNA levels in HUVEC (b) or HDMEC (c) treated or not with 3nM FGF-2 for 48 or 72 h as indicated. GAPDH was used as an internal control. Mean ± SD are presented (n=6; 2 technical replicates of 3 biological replicates excepted for VEGFR-1 and sVEGFR1-ex15 at 48 h n=4; 2 technical replicates of 2 biological replicates, unpaired t test, *p<0.05, **p<0.01, ***p<0.001, ns: not significant)