Swärd K, Dreja K, Hellstrand P
Department of Physiology and Neuroscience, Lund University, Sweden.
J Muscle Res Cell Motil. 1998 Jun;19(5):463-72. doi: 10.1023/a:1005368728376.
The polycations spermine, neomycin and polylysine potentiated Ca(2+)-activated force in beta-escin permeabilized guinea-pig ileum strips. The effect was inhibited by the calmodulin antagonists trifluoperazine, mastoparan and W13. Potentiation was slow or absent in chi-toxin permeabilized strips, indicating dependence on penetration of the polycations into cells. The effects of spermine and neomycin were maintained after extensive permeabilization by beta-escin, which eliminated the contractile effect of GTPgammaS. Replacement of ATP by CTP, which is not a substrate for myosin light chain kinase, inhibited contractile potentiation. Potentiation of Ca(2+)-activated contractions was associated with increased phosphorylation of the myosin regulatory light chains (LC20). A contractile effect of polylysine and neomycin was also seen in Ca(2+)-free medium and after partial LC20 thiophosphorylation, indicating that phosphorylation-independent processes may contribute to the response. Although spermine does not cause contraction in Ca(2+)-free medium at physiological [MgATP], it did so when [MgATP] was lowered to 40 micron. Similar to high-[Mg2+], the rate of contraction on addition of ATP to strips incubated with microcystin-LR in inhibit phosphatase activity was increased by the polycations, but only at [Ca2+] < 0.3 micron. The results suggest that polycations increase Ca(2+)-activated force by inhibiting myosin phosphatase activity, thereby increasing myosin LC20 phosphorylation. However, additional activation mechanisms, evident at low [Ca2+] and at low [ATP] and possibly involving direct activation of myosin, contribute to their effect.
多聚阳离子精胺、新霉素和聚赖氨酸可增强β-七叶皂苷通透的豚鼠回肠条中Ca(2+)激活的张力。钙调蛋白拮抗剂三氟拉嗪、马斯托帕兰和W13可抑制该效应。在几丁质酶通透的条带中,增强作用缓慢或不存在,表明其依赖于多聚阳离子进入细胞。在用β-七叶皂苷进行广泛通透处理后,精胺和新霉素的效应得以维持,而β-七叶皂苷消除了GTPγS的收缩效应。用CTP替代ATP(CTP不是肌球蛋白轻链激酶的底物)可抑制收缩增强。Ca(2+)激活收缩的增强与肌球蛋白调节轻链(LC20)磷酸化增加有关。在无Ca(2+)的培养基中以及部分LC20硫代磷酸化后,也观察到了聚赖氨酸和新霉素的收缩效应,这表明非磷酸化依赖性过程可能参与了该反应。尽管在生理[MgATP]条件下,精胺在无Ca(2+)的培养基中不会引起收缩,但当[MgATP]降至40微摩尔时,它会引起收缩。与高[Mg2+]情况类似,在用微囊藻毒素-LR孵育以抑制磷酸酶活性的条带中加入ATP时,多聚阳离子会增加收缩速率,但仅在[Ca2+]<0.3微摩尔时。结果表明,多聚阳离子通过抑制肌球蛋白磷酸酶活性来增加Ca(2+)激活的张力,从而增加肌球蛋白LC20磷酸化。然而,在低[Ca2+]和低[ATP]时明显存在的额外激活机制,可能涉及肌球蛋白的直接激活,也对其效应有贡献。