ABSTRACT
Objective To investigate the effect of protein kinase B on calcifition of human aorta vascular smooth muscle cells(HASMCs) stimulated by advanced glycation end products (AGEs). Methods HASMCs were cultured in vitro and randomly divided into control group,DMSO group,AGEs group and AGEs+LY294002 group. The calcification of each group was examined by von Kusaa;the expression of protein was detected by west-ern blot and ALP levels in each group by Elisa. Results The expression of bone morphogenetic protein-2(BMP-2)and osteoprotegerin(OPG)in AGEs group was significantly higher than that in control group(P < 0.05). The expression of phosphorylated AKT in AGEs group was significantly higher than that in control group (P < 0.05), and it was time and concentration dependent. Compared with that in AGEs group ,the expression of BMP and OPG in AGEs + LY294002 group was significantly decreased (P < 0.01). Conclusion AKT signaling pathway may play an important role on calcifition of HASMCs caused by AGEs.
ABSTRACT
Objective To investigate the effect of protein kinase B on calcifition of human aorta vascular smooth muscle cells(HASMCs) stimulated by advanced glycation end products (AGEs). Methods HASMCs were cultured in vitro and randomly divided into control group,DMSO group,AGEs group and AGEs+LY294002 group. The calcification of each group was examined by von Kusaa;the expression of protein was detected by west-ern blot and ALP levels in each group by Elisa. Results The expression of bone morphogenetic protein-2(BMP-2)and osteoprotegerin(OPG)in AGEs group was significantly higher than that in control group(P < 0.05). The expression of phosphorylated AKT in AGEs group was significantly higher than that in control group (P < 0.05), and it was time and concentration dependent. Compared with that in AGEs group ,the expression of BMP and OPG in AGEs + LY294002 group was significantly decreased (P < 0.01). Conclusion AKT signaling pathway may play an important role on calcifition of HASMCs caused by AGEs.
ABSTRACT
Objective To investigate the effect of ERK1/2 phosphorylation on the proliferation of human aorta vascular smooth muscle cells (HAVSMCs) stimulated by advanced glycation end products (AGEs) Methods CCK8 was used to test the effect of AGEs with different concentration on the proliferation of HAVSMCs, and the effect of PD98059, a specific inhibitor of ERK1/2, on HAVSMCs proliferation stimulated by AGEs was also detected. Flow Cytometer (FCM) was used to detect the cell cycle transformation induced by AGEs. Western Blot was used to detect the expression of relative proteins. Results 10 mg/L AGEs observably facilitated the proliferation and the DNA synthesis of HAVSMCs and PD98059 (40 umol/L) markedly inhibited the proliferation and cell cycle evolution of HAVSMCs induced by AGEs. Furthermore, ERK1/2 phosphorylation, and PCNA were regulated by AGEs and thus it showed time and dose dependent. Conclusion AGEs participates in the proliferation of HAVSMCs by activating ERK1/2 signal path.