The activation of p38 MAPK limits the abnormal proliferation of vascular smooth muscle cells induced by high sodium concentrations.
作者： YAN WU , JUAN ZHOU , HUAN WANG , YUE WU , QIYUE GAO
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摘要: The aim of the present study was to ascertain whether high sodium levels can directly promote proliferation vascular smooth muscle cells (VSMCs) and elucidate underlying mechanisms. Additional chloride (NaCl) added routine culture medium. Cell evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay 5-ethynyl-2′-deoxyuridine (EdU) incorporation assay. mRNA expression level proliferating cell nuclear antigen (PCNA) measured reverse transcription-quantitative polymerase chain reaction (RT-qPCR). protein PCNA phosphorylated c-Jun amino N-terminal kinase (p-JNK), extracellular signal-regulated 1/2 (p-ERK1/2) p38 mitogen-activated (p-p38 MAPK) were western blot analysis. revealed that Na+ rather than Cl− or osmotic pressure promoted VSMCs. upregulated phosphorylation JNK, ERK1/2 MAPK. inhibition JNK decreased expression. Of note, MAPK using inhibitor, SB203580, increased However, when activated anisomycin, decreased. On whole, our findings demonstrate a relatively per se promotes VSMCs through JNK/ERK1/2/PCNA pathway. At same time, this induction due be maintained at low via activation
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