Cationic liposomes are commonly used as vectors to effectively introduce foreign genes into target cells. In another function, we recently showed that cationic liposomes bound to the mast cell surface suppress the degranulation induced by the cross‐linking of high‐affinity immunoglobulin E receptor in a time‐ and dose‐dependent manner. This suppression is mediated by the impairment of the sustained level of intracellular Ca²⁺ concentration ([Ca²⁺]_i) via the inhibition of store‐operated Ca²⁺ entry. Further, we revealed that the mechanism underlying an impaired [Ca²⁺]_i increase is the inhibition of the activation of the phosphatidylinositol 3‐kinase (PI3K)‐Akt pathway. Yet, how cationic liposomes inhibit the PI3K‐Akt pathway is still unclear. Here, we focused on caveolin‐1, a major component of caveolae, which is reported to be involved in the activation of the PI3K‐Akt pathway in various cell lines. In this study, we showed that caveolin‐1 translocated from the cytoplasm to the plasma membrane after the activation of mast cells and colocalized with the p85 subunit of PI3K, which seemed to be essential for PI3K activity. Meanwhile, cationic liposomes suppressed the translocation of caveolin‐1 to the plasma membrane and the colocalization of caveolin‐1 with PI3K p85 also at the plasma membrane. This finding provides new information for the development of therapies using cationic liposomes against allergies.

中文翻译：

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细胞内caveolin-1分布参与抑制阳离子脂质体对抗原诱导的肥大细胞活化的作用

阳离子脂质体通常用作载体，以有效地将外源基因引入靶细胞。在另一项功能中，我们最近表明，与肥大细胞表面结合的阳离子脂质体以时间和剂量依赖的方式抑制了由高亲和力免疫球蛋白E受体的交联引起的脱颗粒。这种抑制作用是通过抑制贮藏操作的Ca ²⁺进入而损害细胞内Ca ²⁺浓度的持续水平（[Ca ²⁺ ] _i）介导的。此外，我们揭示了[Ca ²⁺ ] _i受损的潜在机制增加是抑制磷脂酰肌醇3激酶（PI3K）-Akt途径的激活。但是，阳离子脂质体如何抑制PI3K-Akt途径仍不清楚。在这里，我们重点研究了小窝蛋白的主要成分小窝蛋白-1，据报道它参与了各种细胞系中PI3K-Akt途径的激活。在这项研究中，我们显示了肥大细胞活化后，caveolin-1从细胞质转移到质膜，并与PI3K的p85亚基共定位，这似乎对PI3K活性至关重要。同时，阳离子脂质体抑制了Caveolin-1向质膜的转运，并抑制了Caveolin-1与PI3K p85在质膜上的共定位。该发现为使用阳离子脂质体抗过敏的疗法的开发提供了新的信息。