Activated VEGFR-1 and VEGFR-2 by UVA both contribute to the survival of keratinocytes via subsequent activation of ERK1/2 and Akt.

<p>(a) Keratinocytes were incubated with or without neutralizing antibodies against VEGFR-1 (A-VEGFR-1, 5 µg/ml) and VEGFR-2 (AVEGFR-2, 5 µg/ml) 24 h after treatment of 0 or 10 J/cm² UVA, and cell apoptosis rate was examined by flow cytometry. (b) Keratinocytes were incubated with neutralizing antibodies against VEGFR-1 (A-VEGFR-1, 5 µg/ml) and/or VEGFR-2 (A-VEGFR-2, 5 µg/ml) 24 h after treatment of 0 or 10 J/cm² UVA, and cell survival was determined by MTT assay. (c) Western blotting detection of cleaved-caspase-3 and Bcl-2 in keratinocytes treated by 10 J/cm2 UVA with or without incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) or VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 24 h. (d) Western blotting detection of phospho-ERK1/2 and phospho-Akt in keratinocytes 12 h after treatment of 10 J/cm² UVA with or without pre-incubation of VEGFR-1 neutralizing antibody (A-VEGFR-1, 5 µg/ml) or VEGFR-2 neutralizing antibody (A-VEGFR-2, 5 µg/ml) for 1 h. GAPDH was served as loading control for protein normalization, UVA: UVA; * <i>P</i><0.05; # <i>P</i><0.01.