Cell Biology International
Cell Biology International
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DOI：
10.1002/(issn)1095-8355
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发表时间：
2019
期刊：
影响因子：
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通讯作者：
Úrsula Maria C. Bastos;I. A. Rosa;J. D. Teixeira;Graciele Gonçalves;Manoel L. Costa;Luis Eduardo M. Quintas;C. Mermelstein
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文献类型：
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作者：
Úrsula Maria C. Bastos;I. A. Rosa;J. D. Teixeira;Graciele Gonçalves;Manoel L. Costa;Luis Eduardo M. Quintas;C. Mermelstein
本研究的目的是测试的假设，增加钠浓度影响血管平滑肌细胞（VSMCs）的迁移表型的血流动力学因素的独立。在以下条件下通过伤口愈合试验评价细胞迁移：高钠（HS，160 mM）和对照（CT，140 mM）。通过膜联蛋白V和碘化丙啶标记评估细胞活力。采用逆转录聚合酶链反应分析环氧合酶-2（考克斯-2）基因表达。通过蛋白质印迹法评估ERK 1/2磷酸化。暴露于HS的VSMCs减少迁移，AT 1 R阻断阻止了这种反应。HS可增加考克斯-2基因表达，而考克斯-2阻断剂可阻止HS诱导的VSMC迁移减少。HS还增加ERK 1/2磷酸化，并且ERK 1/2抑制恢复VSMC迁移以及阻断考克斯-2基因表达。TXA 2受体阻断剂，而不是前列环素受体阻断剂，阻止HS诱导的VSMCs迁移减少。HS通过AT 1 R-ERK 1/2磷酸化增加考克斯-2基因表达，从而减少VSMC的迁移。此外，HS增加考克斯-2似乎可调节TXA 2受体减少VSMCs迁移。
The present study aimed to test the hypothesis that increased sodium concentration affects the migratory phenotype of vascular smooth muscle cells (VSMCs) independently of the haemodynamic factors. Cell migration was evaluated by wound‐healing assay under the following conditions: high sodium (HS, 160 mM) and control (CT, 140 mM). Cell viability was assessed by annexin V and propidium iodide labeling. Cyclooxygenase‐2 (COX‐2) gene expression was analysed by reverse transcription polymerase chain reaction. ERK1/2 phosphorylation was assessed by western blot. Exposure of VSMCs to HS reduced migration, and AT1R blockade prevented this response. HS increased COX‐2 gene expression, and COX‐2 blockade prevented the reduction in VSMC migration induced by HS. HS also increased ERK1/2 phosphorylation, and ERK1/2 inhibition recovered VSMC migration as well as blocked COX‐2 gene expression. The TXA2 receptor blocker, but not the prostacyclin receptor blocker, prevented the HS‐induced VSMCs migration decrease. HS reduces the migration of VSMCs by increasing COX‐2 gene expression via AT1R‐ERK1/2 phosphorylation. In addition, increased COX‐2 by HS seems to modulate the reduction of VSMCs migration by the TXA2 receptor.