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首页> 美国卫生研究院文献>Cell Proliferation >Deletion of a single allele of Cx43 is associated with a reduction in the gap junctional intercellular communication and increased cell proliferation of mouse lung pneumocytes type II
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Deletion of a single allele of Cx43 is associated with a reduction in the gap junctional intercellular communication and increased cell proliferation of mouse lung pneumocytes type II

机译：Cx43的单个等位基因的删除与间隙连接细胞间通讯的减少和II型小鼠肺呼吸细胞的细胞增殖增加有关

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: Connexins (Cx) are proteins that form the gap junctional channels at neighbouring plasma membranes between adjacent cells. Cxs are involved in cell communication, which is reportedly correlated with cell proliferation and differentiation. Alterations in connexin expression and/or gap junctional intercellular communication (GJIC) capacity have long been postulated to be important in a number of pathological conditions including cancer. This study was performed to determine the consequences of the deletion of a single allele of (Cx43 gene) in Alveolar Type II cells (APTIIs), and its impact on GJIC and cell proliferation. : In order to do so, APTIIs from wild type (Cx43 ) and heterozygous (Cx43 ) mice were harvested and cultured for 4 days. The GJIC capacity was evaluated by scrape‐loading method, with the transfer of lucifer yellow dye. The expression of Cx43 was evaluated by immunofluorescence method and Western blotting. Cell proliferation was evaluated by 3‐(4,5‐dimethylthazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide assay. : It was observed that GJIC capacity was significantly reduced and cell proliferation index was significantly higher in Cx43 cells compared to Cx43 cells. : These results show that knocking out one allele of Cx43 leads to a lower cell to cell communication capacity, and consequently induces a higher cell proliferation. Because chemically induced lung adenomas in mice are known to originate from APTIIs, these alterations may play a critical role in their susceptibility to lung carcinogenesis.
机译：：连接蛋白（Cx）是在相邻细胞之间的相邻质膜上形成间隙连接通道的蛋白质。 Cxs参与细胞通讯，据报道与细胞增殖和分化有关。长期以来，人们推测连接蛋白表达和/或间隙连接细胞间通讯（GJIC）能力的改变在包括癌症在内的许多病理状况中都是重要的。进行这项研究是为了确定II型肺泡细胞（APTIIs）中（Cx43基因）单个等位基因缺失的后果及其对GJIC和细胞增殖的影响。 ：为此，收获了来自野生型（Cx43）和杂合型（Cx43）小鼠的APTII，并培养了4天。 GJIC容量通过刮涂法评估，并带有荧光素黄染料的转移。通过免疫荧光法和蛋白质印迹法评估Cx43的表达。细胞增殖通过3-（4,5-二甲基噻唑-2-基）-2-5-二苯基四唑溴化物测定进行评估。 ：观察到，与Cx43细胞相比，Cx43细胞的GJIC容量显着降低并且细胞增殖指数显着更高。 ：这些结果表明，敲除Cx43的一个等位基因会导致较低的细胞间通讯能力，从而诱导较高的细胞增殖。因为已知小鼠中化学诱导的肺腺瘤起源于APTII，所以这些改变可能在其对肺癌发生的敏感性中起关键作用。

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