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首页> 外文期刊>Endothelium: Journal of endothelial cell research >TGF-beta1 induces an accumulation of connexin43 in a lysosomal compartment in endothelial cells.
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TGF-beta1 induces an accumulation of connexin43 in a lysosomal compartment in endothelial cells.

机译：TGF-beta1诱导连接蛋白在内皮细胞的溶酶体区室中的积累。

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摘要

We have been studying the relationships between cell growth and the expression of the gap junction protein Connexin43 (Cx43) in cultured bovine aortic endothelial cells (BAEC). As part of these studies, we examined the effect of the growth inhibitory cytokine TGF-beta1 on Cx43 expression. We have shown recently that TGF-beta treatment increases Cx43 mRNA and synthesis, content, and half-life of the protein within 24 h, which leads, over the course of days, to an accumulation of Cx43 in large, intensely immunostaining vesicles, filling much of the perinuclear cytoplasmic space. In the current study, based on their distribution and markers, we identified these vesicles as lysosomes/autophagosomes. Cx43 immunostaining and staining with a fluorescent probe for acidic compartments are coincident, as retention of a fluorescent-labeled low-density lipoprotein occurs in a similar pattern and the same staining pattern can be detected in the treated cells using other markers for lysosomal compartments. TEM revealed prominent lysosomal figures with considerable heterogeneous material. After withdrawal of TGF-beta, the accumulated Cx43 was cleared only slowly, with some brightly immunoreactive cells remaining even after 72 h. The prolonged appearance (based on immunoreactivity in situ and in immunoblots) of intact vesicular Cx43 in the treated cells suggests decreased degradation, resulting from impaired lysosomal activity. These data not only emphasize the importance of the lysosome in connexin degradation, but also show that TGF-beta can cause an alteration in lysosomal functioning, with implications for cellular metabolism.
机译：我们一直在研究牛主动脉内皮细胞（BAEC）中细胞生长与间隙连接蛋白Connexin43（Cx43）表达之间的关系。作为这些研究的一部分，我们检查了生长抑制性细胞因子TGF-beta1对Cx43表达的影响。我们最近发现，TGF-β处理可在24小时内增加Cx43 mRNA的合成以及该蛋白的合成，含量和半衰期，这导致几天之内Cx43在大量高度免疫染色的囊泡中积聚，大部分核周细胞质空间。在当前的研究中，基于它们的分布和标记，我们将这些囊泡鉴定为溶酶体/自噬体。酸性隔室的Cx43免疫染色和荧光探针染色是一致的，因为荧光标记的低密度脂蛋白的保留以相似的模式发生，并且可以使用其他溶酶体隔室标记物在处理过的细胞中检测到相同的染色模式。 TEM显示出明显的溶酶体图，具有相当多的异质物质。撤回TGF-beta后，积累的Cx43仅缓慢清除，即使72小时后仍保留了一些明亮的免疫反应性细胞。在处理过的细胞中完整囊泡Cx43的延长出现时间（基于原位和免疫印迹）表明降解降低，这是由于溶酶体活性受损所致。这些数据不仅强调了溶酶体在连接蛋白降解中的重要性，而且还表明TGF-β可以引起溶酶体功能的改变，从而影响细胞代谢。

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