Helicobacter pylori inhibits gastric cell cycle progression
Helicobacter pylori inhibits gastric cell cycle progression
复制标题
DOI：
10.1016/s1286-4579(00)01270-3
复制
发表时间：
2000-08-01
影响因子：
5.8
通讯作者：
Ashktorab, H
中科院分区：
文献类型：
--
作者：
Ahmed, A;Smoot, D;Ashktorab, H
胃粘膜幽门螺杆菌感染与胃上皮细胞增殖的变化有关。体外研究表明，暴露于H。pylori抑制胃细胞增殖。本研究旨在探讨在存在和不存在H.幽门。非同步化和同步化的胃上皮细胞系AGS和KatoIII暴露于H。pylori在24小时内。通过流式细胞术使用碘化丙啶（PI），并通过分析细胞周期蛋白E，p21，和p53蛋白表达使用蛋白质印迹法测定细胞周期进程。在没有H。pylori感染后，流式细胞仪分析显示，分别有40、45和15%的未同步化AGS细胞处于G（0）-G（1）、S和G（2）-M期。AGS细胞在H. pylori感染后24 h，S期细胞减少10%，G（0）-G（1）期细胞增加17%。缺失p53基因的KatoIII细胞对H.幽门。G1/S期同步化的AGS细胞与含H. pylori感染后24 h，G（1）期细胞数较对照组明显增加（25%，P < 0.05）。相反，对照细胞能够通过S期。H. pylori对AGS细胞周期的影响与p53和p21表达的增加有关。H. pylori 24 h。研究表明，H.幽门螺杆菌诱导的体外生长抑制主要在G（0）-G（1）检查点。我们的结果表明p53可能在H中很重要。幽门螺杆菌诱导的细胞周期停滞。这些结果支持：在G（2）细胞周期阻滞中发挥作用的细胞周期蛋白依赖性激酶抑制剂。pylori及其参与改变细胞周期中的调节蛋白p53、p21和细胞周期蛋白E。(C)2000年，Elsevier SAS科学与医学版。
Helicobacter pylori infection of the gastric mucosa is associated with changes in gastric epithelial cell proliferation. In vitro studies have shown that exposure to H. pylori inhibits proliferation of gastric cells. This study sought to investigate the cell cycle progression of gastric epithelial cell lines in the presence and absence of H. pylori. Unsynchronized and synchronized gastric epithelial cell lines AGS and KatoIII were exposed to H. pylori over a 24-h period. Cell cycle progression was determined by flow cytometry using propidium iodide (PI), and by analysis of cyclin E, p21, and p53 protein expression using Western blots. In the absence of H. pylori 40, 45, and 15 % of unsynchronized AGS cells were in G(0)-G(1), S, and G(2)-M phases, respectively, by flow cytometry analysis. When AGS cells were cultured in the presence of H. pylori, the S phase decreased 10% and the G(0)-G(1) phase increased 17% after 24 h compared with the controls. KatoIII cells, which have a deleted p53 gene, showed little or no response to H. pylori. When G1/S synchronized AGS cells were incubated with media containing H. pylori, the G(1) phase increased significantly (25%, P < 0.05) compared with controls after 24 h. In contrast, the control cells were able to pass through S phase. The inhibitory effects of H. pylori on the cell cycle of AGS cells were associated with a significant increase in p53 and p21 expression after 24 h. The expression of cyclin E was downregulated in AGS cells following exposure of AGS cells to H. pylori for 24 h. This study shows that H. pylori-induced growth inhibition in vitro is predominately at the G(0)-G(1) checkpoint. Our results suggest that p53 may be important in H. pylori-induced cell cycle arrest. These results support: a role for cyclin-dependent kinase inhibitors in the G(2) cell cycle arrest exerted by fi. pylori and its involvement in changing the regulatory proteins, p53, p21, and cyclin E in the cell cycle. (C) 2000 Editions scientifiques et medicales Elsevier SAS.