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首页> 外文期刊>Cell communication & adhesion >Ischemia-Induced Cleavage of Cadherins in NRK Cells is not Sufficient for β-catenin Transcriptional Activity
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Ischemia-Induced Cleavage of Cadherins in NRK Cells is not Sufficient for β-catenin Transcriptional Activity

机译：缺血诱导的NRK细胞中钙黏着蛋白的裂解不足以实现β-catenin转录活性

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摘要

Although ischemia is associated with disruption of cadherinβ-mediated adhesion in renal cell lines, the impact of decreased cadherin function on the transcriptional activity of β-catenin remains poorly defined. In these studies, we used a simulated ischemia model in normal rat kidney (NRK) cells to disrupt cadherin function. Cell viability; cadherin/catenin expression, function, and localization; and β-catenin-mediated transcriptional activity were assessed during ischemia/reperfusion. Following 6 hr of ischemia, a decrease in the expression of E- and N-cadherin was seen that correlated with altered cell morphology indicative of decreased intercellular adhesion. While ischemia was associated with activation of glycogen synthase kinase 3 beta (GSK-3), this did not correlate with increased phosphorylation of β-catenin as assessed by Western blots using phosphoryl-specific antibodies. β-Catenin was not localized to the nucleus by immunofluorescence in ischemic NRK cells, but rather a strong perinuclear signal was seen in reperfused cells. This was consistent with the finding that neither ischemia nor reperfusion activated the transcriptional activity of β-catenin as assessed by the TCF-optimal promoter (TOPFlash) construct. However, NRK cells possess a competent Wnt pathway, as challenge with lithium chloride elicited a ten-fold increase in luciferase activity. These results suggest that ischemia-induced disruption of cadherin/catenin complexes is not sufficient to stimulate β-catenin transcriptional activity in NRK cells.
机译：尽管缺血与肾细胞系中钙黏着蛋白介导的粘附破坏有关，但钙黏着蛋白功能降低对β-连环蛋白转录活性的影响仍然不清楚。在这些研究中，我们在正常大鼠肾脏（NRK）细胞中使用了模拟的缺血模型来破坏钙黏着蛋白功能。细胞活力;钙粘蛋白/连环蛋白的表达，功能和定位;在缺血/再灌注期间评估β-catenin介导的转录活性。缺血6小时后，发现E-和N-钙粘着蛋白的表达降低与细胞形态改变相关，表明细胞间粘附降低。虽然缺血与糖原合酶激酶3β（GSK-3）的激活相关，但如使用磷酸化特异性抗体的Western印迹所评估，这与β-catenin磷酸化的增加无关。 β-连环蛋白在缺血性NRK细胞中未通过免疫荧光定位于细胞核，但在再灌注细胞中却观察到了强烈的核周信号。这与通过TCF-最佳启动子（TOPFlash）构建物评估的缺血或再灌注均未激活β-catenin的转录活性的发现是一致的。但是，NRK细胞具有胜任的Wnt途径，因为氯化锂的激发引起萤光素酶活性增加了十倍。这些结果表明，缺血诱导的钙粘蛋白/连环蛋白复合物的破坏不足以刺激NRK细胞中的β-连环蛋白转录活性。

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