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首页> 外文期刊>American Journal of Physiology >Intracellular signal transduction for migration and actin remodeling in vascular smooth muscle cells after sphingosylphosphorylcholine stimulation.
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Intracellular signal transduction for migration and actin remodeling in vascular smooth muscle cells after sphingosylphosphorylcholine stimulation.

机译：鞘氨醇磷酸胆碱刺激后血管平滑肌细胞迁移和肌动蛋白重塑的细胞内信号转导。

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摘要

Molecular mechanisms underlying migration of vascular smooth muscle cells (VSMCs) toward sphingosylphosphorylcholine (SPC) were analyzed in light of the hypothesis that remodeling of the actin cytoskeleton should be involved. After SPC stimulation, mitogen-activated protein kinases (MAPKs), including p38 MAPK (p38) and p42/44 MAPK (p42/44), were found to be phosphorylated. Migration of cells toward SPC was reduced in the presence of SB-203580, an inhibitor of p38, but not PD-98059, an inhibitor of p42/44. Pertussis toxin (PTX), a Gi protein inhibitor, induced an inhibitory effect on p38 phosphorylation and VSMC migration. Myosin light chain (MLC) phosphorylation occurred after SPC stimulation with or without pretreatment with SB-203580 or PTX. The MLC kinase inhibitor ML-7 and the Rho kinase inhibitor Y-27632 inhibited MLC phosphorylation but only partially inhibited SPC-directed migration. Complete inhibition was achieved with the addition of SB-203580. After SPC stimulation, the actin cytoskeleton formed thick bundles of actin filaments around the periphery of cells, and the cells were surrounded by elongated filopodia, i.e., magunapodia. The peripheral actin bundles consisted of alpha- and beta-actin, but magunapodia consisted exclusively of beta-actin. Such a remodeling of actin was reversed by addition of SB-203580 and PTX, but not ML-7 or Y-27632. Taken together, our biochemical and morphological data confirmed the regulation of actin remodeling and suggest that VSMCs migrate toward SPC, not only by an MLC phosphorylation-dependent pathway, but also by an MLC phosphorylation-independent pathway.
机译：根据假说肌动蛋白细胞骨架应参与重塑的假设，分析了血管平滑肌细胞（VSMC）向鞘氨醇磷酸胆碱（SPC）迁移的分子机制。在SPC刺激后，发现包括p38 MAPK（p38）和p42 / 44 MAPK（p42 / 44）在内的丝裂原活化蛋白激酶（MAPK）被磷酸化。在存在p38抑制剂SB-203580而不是p42 / 44抑制剂PD-98059的情况下，细胞向SPC的迁移减少。 Gi蛋白抑制剂百日咳毒素（PTX）诱导了对p38磷酸化和VSMC迁移的抑制作用。 SPC刺激后，无论是否使用SB-203580或PTX预处理，均会发生肌球蛋白轻链（MLC）磷酸化。 MLC激酶抑制剂ML-7和Rho激酶抑制剂Y-27632抑制MLC磷酸化，但仅部分抑制SPC定向迁移。通过添加SB-203580达到完全抑制。在SPC刺激后，肌动蛋白细胞骨架在细胞周围形成了厚厚的肌动蛋白丝束，并且细胞被细长的丝状伪足（即真足伪足）所包围。外周肌动蛋白束由α-肌动蛋白和β-肌动蛋白组成，但magunapodia完全由β-肌动蛋白组成。通过添加SB-203580和PTX，而不是ML-7或Y-27632，可以逆转肌动蛋白的这种重塑。综上所述，我们的生化和形态学数据证实了肌动蛋白重塑的调控，并暗示VSMC不仅通过MLC磷酸化依赖性途径，而且通过MLC磷酸化依赖性途径向SPC迁移。

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