Tissue remodeling during tumor necrosis factor-induced apoptosis in LLC-PK1 renal epithelial cells.
Tissue remodeling during tumor necrosis factor-induced apoptosis in LLC-PK1 renal epithelial cells.
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DOI：
10.1152/ajprenal.1996.270.5.f869
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发表时间：
1996-05
期刊：
影响因子：
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通讯作者：
A. P. Soler;James M. Mullin;K. Knudsen;C. Marano
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文献类型：
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作者：
A. P. Soler;James M. Mullin;K. Knudsen;C. Marano
细胞因子肿瘤坏死因子-α（TNF）增加融合肾上皮LLC-PK1细胞的凋亡频率，这种作用可以被抗TNFR1单克隆抗体阻断。然而，有没有可见的“洞”的细胞片作为TNF诱导的凋亡的结果。相反，一个显着的组织重建发生在响应TNF诱导的细胞凋亡。凋亡细胞被重新定位的相邻细胞包围和吞噬，以独特的"玫瑰花结"模式分布。钙粘蛋白-连环蛋白细胞间粘附分子、紧密连接相关蛋白ZO-1和肌动蛋白在凋亡细胞和相邻细胞之间的接触部位聚集。用细胞松弛素B预处理防止了钙粘蛋白-连环蛋白和ZO-1在凋亡位点的积累，并导致TNF处理的细胞片中的微观孔。我们的研究结果表明，肾上皮细胞可以容纳增加的凋亡频率，并仍然保持其完整性的组织重塑机制，涉及钙粘蛋白-连环蛋白粘附分子，紧密连接蛋白，肌动蛋白丝。
The cytokine tumor necrosis factor-alpha (TNF) increases the frequency of apoptosis in confluent renal epithelial LLC-PK1 cells, an effect that can be blocked by an anti-TNFR1 monoclonal antibody. However, there were no visible "holes" in the cell sheet as a result of TNF-induced apoptosis. Instead a striking tissue remodeling occurred in response to the TNF-induced apoptosis. Apoptotic cells became surrounded and engulfed by repositioned neighboring cells distributed in a distinct "rosette" pattern. The cadherin-catenin cell-cell adhesion molecules, the tight junction-associated protein ZO-1, and actin accumulated at the sites of contact between apoptotic and neighboring cells. Pretreatment with cytochalasin B prevented the accumulation of cadherins-catenins and ZO-1 at the sites of apoptosis and resulted in microscopic holes in the TNF-treated cell sheet. Our results indicate that a renal epithelium can accommodate an increased frequency of apoptosis and still maintain its integrity by mechanisms of tissue remodeling involving the cadherin-catenin adhesion molecules, tight junctional proteins, and actin filaments.