Basic Study
Copyright ©The Author(s) 2015.
World J Transl Med. Dec 12, 2015; 4(3): 101-112
Published online Dec 12, 2015. doi: 10.5528/wjtm.v4.i3.101
Figure 3
Figure 3 Involvement of p38 mitogen-activated protein kinase in the phenotype regulation of human vascular endothelial cells. A: Type-II ESdECs were transfected with either an RGS5 expression vector or an empty vector by nucleofection and subjected to Western blotting using indicated antibodies after 3 or 4 d; B: Type-II ESdECs were treated with either 0.1% DMSO, a p38 MAPK inhibitor (10 μmol/L) or a JNK inhibitor (10 μmol/L) for three days and subjected to co-cultures with human aortic smooth muscle cells (n = 3, AV ± SD); C: Type-II ESdECs were treated by a p38 MAPK inhibitor (10 μmol/L). Next day, RGS5 expressions were examined by qRT-PCR (n = 4, AV ± SD). RGS5: Regulator of G-protein signaling 5; ESdECs: Embryonic stem cells-derived vascular endothelial cells; DMSO: Dimethylsulfoxide; JNK: Jun N-terminal kinase; MAPK: Mitogen-activated protein kinase; qRT-PCR: Quantitative real-time polymerase chain reaction; HUVEC: Human umbilical vein endothelial cells.