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Cell membrane disruption stimulates cAMP and Ca2+?signaling to potentiate cell membrane resealing in neighboring cells

机译:细胞膜破坏刺激cAMP和Ca2 +信号转导增强邻近细胞中的细胞膜重封

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Disruption of cellular plasma membranes is a common event in many animal tissues, and the membranes are usually rapidly resealed. Moreover, repeated membrane disruptions within a single cell reseal faster than the initial wound in a protein kinase A (PKA)- and protein kinase C (PKC)-dependent manner. In addition to wounded cells, recent studies have demonstrated that wounding of Madin-Darby canine kidney (MDCK) cells potentiates membrane resealing in neighboring cells in the short-term by purinergic signaling, and in the long-term by nitric oxide/protein kinase G signaling. In the present study, real-time imaging showed that cell membrane disruption stimulated cAMP synthesis and Ca2+?mobilization from intracellular stores by purinergic signaling in neighboring MDCK cells. Furthermore, inhibition of PKA and PKC suppressed the ATP-mediated short-term potentiation of membrane resealing in neighboring cells. These results suggest that cell membrane disruption stimulates PKA and PKC via purinergic signaling to potentiate cell membrane resealing in neighboring MDCK cells.
机译:细胞质膜破裂是许多动物组织中的常见事件,通常会迅速将其重新密封。而且,单个细胞内重复的膜破坏以依赖蛋白激酶A(PKA)和依赖蛋白激酶C(PKC)的方式重新密封的速度比初始伤口快。除了受伤的细胞外,最近的研究表明,Madin-Darby犬肾(MDCK)细胞的受伤在短期内通过嘌呤能信号传导增强了邻近细胞的膜重封,在长期内通过一氧化氮/蛋白激酶G增强了膜重封。信号。在本研究中,实时成像显示细胞膜破裂通过邻近MDCK细胞的嘌呤能信号传导刺激了cAMP的合成和细胞内Ca2 +的迁移。此外,对PKA和PKC的抑制作用抑制了ATP介导的邻近细胞膜重封的短期增强。这些结果表明细胞膜破坏通过嘌呤能信号传导刺激PKA和PKC,以增强相邻MDCK细胞中细胞膜的重密封。

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