Factors derived from preeclamptic placentas perturb polarity protein PARD-3 expression and distribution in endothelial cells.
Factors derived from preeclamptic placentas perturb polarity protein PARD-3 expression and distribution in endothelial cells.
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DOI：
10.1177/1933719110382920
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发表时间：
2011-02
期刊：
影响因子：
--
通讯作者：
Wang Y
中科院分区：
文献类型：
--
作者：
Zhao J;Gu Y;Fan R;Groome LJ;Wang Y
本研究旨在检测（1）极性蛋白分配缺陷3（PARD-3）是否在内皮细胞（EC）中表达并有助于内皮屏障的完整性，以及（2）PARD-3表达和分布的改变是否与先兆子痫（PE）胎盘因子诱导的内皮连接蛋白VE-钙粘蛋白表达紊乱相关。用免疫荧光染色和Western blot方法检测汇合的EC和正常及PE胎盘条件培养液（CM）处理的EC中PARD-3和VE-钙粘蛋白的表达。用免疫沉淀和免疫印迹法检测PARD-3/VE-钙粘蛋白、PARD-3/非典型蛋白激酶C（aPKCλ）和VE-钙粘蛋白/aPKCλ之间的蛋白质-蛋白质相互作用。与VE-钙粘蛋白类似，PARD-3定位于对照EC中的细胞接触处。与未处理的对照组相比，PE-CM处理2小时的细胞中PARD-3和VE-钙粘蛋白的表达均显著降低，但在正常CM处理的细胞中没有降低。用PE-CM处理24小时后，细胞中VE-钙粘蛋白和PARD-3的细胞溶胶染色明显。在PE-CM处理的细胞中检测到PARD-3/VE-钙粘蛋白和PARD-3/aPKCλ复合物，而在未处理的对照细胞和恢复后的细胞中未检测到PARD-3/VE-钙粘蛋白和PARD-3/aPKCλ复合物。对照组和恢复组细胞中检测到VE-钙粘蛋白/aPKCλ复合物，而PE-CM处理组细胞中未检测到。极性蛋白PARD-3定位于细胞接触处。PE胎盘源性因子不仅干扰连接蛋白VE-钙粘蛋白的分布，而且干扰极性蛋白PARD-3在EC中的表达和分布。胎盘CM处理的ECs中PARD-3/VE-钙粘蛋白和PARD-3/aPKCλ复合物的形成表明胎盘来源的因子可以干扰ECs中连接蛋白和极性蛋白的功能。
This study aimed to examine (1) whether polarity protein partitioning defective-3 (PARD-3) was expressed in endothelial cells (ECs) and contributed to endothelial barrier integrity and (2) whether altered PARD-3 expression and distribution were associated with disturbed endothelial junction protein VE-cadherin expression induced by factors derived from preeclamptic (PE) placentas. PARD-3 and VE-cadherin expressions were examined by immunofluorescent staining and Western blot in confluent ECs and in ECs treated with normal and PE placental conditioned medium (CM). Protein-protein interactions between PARD-3/VE-cadherin, PARD-3/ atypical protein kinase C (aPKCλ), and VE-cadherin/aPKCλ were examined by immuno-precipitation and immunobloting. Similar to VE-cadherin, PARD-3 is localized at the cell contacts in control ECs. Both PARD-3 and VE-cadherin expressions were markedly reduced in cells treated with PE-CM for 2h, but not in cells treated with normal-CM compared to non-treated controls. Cytosol staining of VE-cadherin and PARD-3 was pronounced in cells after 24h treatment with PE-CM. PARD-3/VE-cadherin and PARD-3/aPKCλ complexes were detected in PE-CM treated cells, but not in untreated control cells and in cells after recovery. In contrast, VE-cadherin/aPKCλ complex was detected in control cells and in cells after recovery, but not in PE-CM treated cells. Polarity protein PARD-3 is localized at cell contacts. Factors-derived from PE placentas not only interrupt junction protein VE-cadherin distribution, but also perturb polarity protein PARD-3 expression and distribution in ECs. The results of PARD-3/VE-cadherin and PARD-3/aPKCλ complexes formation in cells treated with placental CM suggest that factors-derived from placenta could interfere both junction protein and polarity protein functions in ECs.
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DOI：
10.1083/jcb.152.6.1183
发表时间：
2001-03-19
期刊：
The Journal of cell biology
影响因子：
--
作者：
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DOI：
10.1016/j.cub.2009.05.065
发表时间：
2009-07-14
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Current biology : CB
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