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首页> 外文期刊>American Journal of Physiology >Sphingosylphosphorylcholine stimulates mitogen-activated protein kinase via a Ca2+-dependent pathway.
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Sphingosylphosphorylcholine stimulates mitogen-activated protein kinase via a Ca2+-dependent pathway.

机译：鞘氨醇磷酸胆碱通过Ca 2+依赖性途径刺激丝裂原活化的蛋白激酶。

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摘要

In cultured porcine aortic smooth muscle cells, sphingosylphosphorylcholine (SPC), ATP, or bradykinin (BK) induced a rapid dose-dependent increase in the cytosolic Ca2+ concentration ([Ca2+]i) and also stimulated inositol 1,4,5-trisphosphate (IP3) generation. Pretreatment of cells with pertussis toxin blocked the SPC-induced IP3 generation and [Ca2+]i increase but had no effect on the action of ATP or BK. In addition, SPC stimulated the mitogen-activated protein kinase (MAPK) and increased DNA synthesis, whereas neither ATP nor BK produced such effects. Both the SPC-induced MAPK activation and DNA synthesis were pertussis toxin sensitive. SPC-induced MAPK activation was blocked by treatment of cells with the phospholipase C inhibitor, U-73122, or the intracellular Ca2+-ATPase inhibitor, thapsigargin, but not by removal of extracellular Ca2+. Lysophosphatidic acid induced cellular responses similar to SPC in a pertussis toxin-sensitive manner in terms of [Ca2+]i increase, IP3 generation, MAPK activation, and DNA synthesis. Platelet-derived growth factor (PDGF) also induced a [Ca2+]i increase, MAPK activation, and DNA synthesis in the same cells; however, the PDGF-induced MAPK activation was not sensitive to pertussis toxin and changes in [Ca2+]i. SPC-induced MAPK activation was inhibited by pretreatment of cells with staurosporine, W-7, or calmidazolium. Our results suggest that, in porcine aortic smooth muscle cells, MAPK is not activated by the increase in [Ca2+]i unless a pertussis toxin-sensitive G protein is simultaneously stimulated, indicating the role of Ca2+ in pertussis toxin-sensitive G protein-mediated MAPK activation.
机译：在培养的猪主动脉平滑肌细胞中，鞘氨醇磷酸胆碱（SPC），ATP或缓激肽（BK）引起胞浆Ca2 +浓度（[Ca2 +] i）的剂量依赖性快速增加，并且还刺激了1,4,5-三磷酸肌醇（ IP3）生成。用百日咳毒素预处理细胞可以阻止SPC诱导的IP3生成，[Ca2 +] i升高，但对ATP或BK的作用没有影响。此外，SPC刺激有丝分裂原激活的蛋白激酶（MAPK）并增加DNA合成，而ATP和BK均不产生这种作用。 SPC诱导的MAPK激活和DNA合成均对百日咳毒素敏感。通过用磷脂酶C抑制剂U-73122或细胞内Ca2 + -ATPase抑制剂thapsigargin处理细胞可阻止SPC诱导的MAPK活化，但不能通过去除细胞外Ca2 +来阻止。在[Ca2 +] i增加，IP3生成，MAPK激活和DNA合成方面，溶血磷脂酸以百日咳毒素敏感的方式诱导类似于SPC的细胞应答。血小板衍生的生长因子（PDGF）也诱导了同一细胞中[Ca2 +] i的增加，MAPK活化和DNA合成。然而，PDGF诱导的MAPK激活对百日咳毒素和[Ca2 +] i的变化不敏感。 SPC诱导的MAPK激活被星形孢菌素，W-7或卡地咪唑预处理而被抑制。我们的研究结果表明，在猪主动脉平滑肌细胞中，除非同时刺激百日咳毒素敏感的G蛋白，否则[Ca2 +] i的增加不会激活MAPK，这表明Ca2 +在百日咳毒素敏感的G蛋白介导的作用中MAPK激活。

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