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GW24-e2369 Aliskiren inhibits proliferation of vascular smooth muscle cells induced by platelet-derived growth factor-BB via extracellular regulated protein kinases signal pathway
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Objectives
To identify the effect of direct renin inhibitor aliskiren on proliferation of vascular smooth muscle cells (VSMCs) induced by PDGF-BB, and study the mechanism of this effect.
Methods
The rats thoracic aorta smooth muscle cells (A10 cells) were used in the study, the effects of different concentrations of aliskiren and PDGF-BB as well as different stimulus durations of 10 μmol/L aliskiren and 20 ng/mL PDGF-BB stimulated on VSMCs proliferation was observed by [3H]-TdR; ERK, p-ERK and β-actin were assessed by immunoblotting.
Results
PDGF-BB could induce A10 cell proliferation, and the ratio of cell proliferation treated with 20 ng/mL PDGF-BB was (145.50 ± 10.51) % (P < 0.05) compared with the control group. Aliskiren could suppress PDGF-BB-induced proliferation of VSMCs, the ratio of cell proliferation treated with 20 ng/mL PDGF-BB plus 10 μmol/L aliskiren was (44.65 ± 24.42) % (P < 0.05) which is reduce compared with the cells treated with 20 ng/mL PDGF-BB alone. The effect of aliskiren ; immunoblotting showed that the effect of aliskiren on VSMC proliferation induced by PDGF-BB might be via ERK1/2 signal pathway.
Conclusions
Aliskiren suppressed PDGF-BB-induced proliferation of VSMCs, via ERK1/2 signal pathway.
Title: GW24-e2369 Aliskiren inhibits proliferation of vascular smooth muscle cells induced by platelet-derived growth factor-BB via extracellular regulated protein kinases signal pathway
Description:
Objectives
To identify the effect of direct renin inhibitor aliskiren on proliferation of vascular smooth muscle cells (VSMCs) induced by PDGF-BB, and study the mechanism of this effect.
Methods
The rats thoracic aorta smooth muscle cells (A10 cells) were used in the study, the effects of different concentrations of aliskiren and PDGF-BB as well as different stimulus durations of 10 μmol/L aliskiren and 20 ng/mL PDGF-BB stimulated on VSMCs proliferation was observed by [3H]-TdR; ERK, p-ERK and β-actin were assessed by immunoblotting.
Results
PDGF-BB could induce A10 cell proliferation, and the ratio of cell proliferation treated with 20 ng/mL PDGF-BB was (145.
50 ± 10.
51) % (P < 0.
05) compared with the control group.
Aliskiren could suppress PDGF-BB-induced proliferation of VSMCs, the ratio of cell proliferation treated with 20 ng/mL PDGF-BB plus 10 μmol/L aliskiren was (44.
65 ± 24.
42) % (P < 0.
05) which is reduce compared with the cells treated with 20 ng/mL PDGF-BB alone.
The effect of aliskiren ; immunoblotting showed that the effect of aliskiren on VSMC proliferation induced by PDGF-BB might be via ERK1/2 signal pathway.
Conclusions
Aliskiren suppressed PDGF-BB-induced proliferation of VSMCs, via ERK1/2 signal pathway.
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