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首页> 外文期刊>The journal of sexual medicine >Derangements in endothelial cell-to-cell junctions involved in the pathogenesis of hypercholesterolemia-induced erectile dysfunction.
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Derangements in endothelial cell-to-cell junctions involved in the pathogenesis of hypercholesterolemia-induced erectile dysfunction.

机译：高胆固醇血症引起的勃起功能障碍发病机制中涉及的内皮细胞间连接紊乱。

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INTRODUCTION: Endothelial cell-to-cell junctions are crucial for vascular formation, networking, and remodeling of blood vessels as well as for inducing and integrating intracellular signals. AIM: We investigated the differential expression and distribution of endothelial cell-to-cell junction proteins in the penis of mice with hypercholesterolemia-induced erectile dysfunction. METHODS: Two-month-old C57BL/6J mice were fed a diet containing 4% cholesterol and 1% cholic acid, and age-matched control animals were fed a normal diet, for 3 months. We performed dual priming oligonucleotide (DPO)-based multiplex polymerase chain reaction (PCR) (Seegene, Seoul, Korea) to screen the differential gene expression of 21 endothelial cell-to-cell junctions. MAIN OUTCOME MEASURES: At 5 months, erectile function was measured by electrical stimulation of the cavernous nerve, and the penis was harvested and stained with antibody to claudin-5, vascular endothelial (VE)-cadherin, and platelet/endothelial cell adhesion molecule (PECAM)-1 (N = 8 per group). Cavernous specimens from a separate group of animals were used for claudin-5, VE-cadherin, and PECAM-1 reverse transcriptase-PCR and Western blot analysis. RESULTS: Erectile function was significantly lower in hypercholesterolemic mice than in controls. DPO-based multiplex PCR revealed a profound decrease in the gene expression of endothelium-specific cell-to-cell junction proteins, including claudin-5, VE-cadherin, and PECAM-1, in hypercholesterolemic mice compared with that in controls. The expression of claudin-5, VE-cadherin, and PECAM-1 protein evaluated by Western blot or immunohistochemistry was significantly lower in hypercholesterolemic mice than in controls. These endothelial cell-to-cell junction proteins were more sparsely distributed in the endothelium of cavernous sinusoids than in the endothelium of cavernous artery and dorsal blood vessels. CONCLUSION: Down-regulation of the endothelial cell-to-cell junctions and decreased endothelial content in the corpus cavernosum might play a major role in the deterioration of erectile function in hypercholesterolemic mice.
机译：简介：内皮细胞间连接对于血管形成，网络连接和血管重塑以及诱导和整合细胞内信号至关重要。目的：我们研究了高胆固醇血症引起的勃起功能障碍小鼠的阴茎中内皮细胞间连接蛋白的差异表达和分布。方法：给两个月大的C57BL / 6J小鼠喂食含4％胆固醇和1％胆酸的饮食，与年龄匹配的对照组动物喂食正常饮食3个月。我们进行了基于双引物寡核苷酸（DPO）的多重聚合酶链反应（PCR）（Seegene，首尔，韩国）以筛选21种内皮细胞间连接的差异基因表达。主要观察指标：5个月后，通过电刺激海绵状神经测量勃起功能，收集阴茎并用claudin-5抗体，血管内皮（钙）钙粘蛋白和血小板/内皮细胞粘附分子染色（ PECAM）-1（每组N = 8）。来自另外一组动物的海绵状标本用于claudin-5，VE-钙粘着蛋白和PECAM-1逆转录酶-PCR和蛋白质印迹分析。结果：高胆固醇血症小鼠的勃起功能明显低于对照组。基于DPO的多重PCR显示，与对照组相比，高胆固醇血症小鼠的内皮特异性细胞间连接蛋白（包括claudin-5，VE-cadherin和PECAM-1）的基因表达大大降低。通过Western印迹或免疫组织化学评估的claudin-5，VE-cadherin和PECAM-1蛋白的表达在高胆固醇血症小鼠中明显低于对照组。这些内皮细胞间连接蛋白比海绵状动脉和背侧血管内皮更稀疏地分布在海绵窦中。结论：海绵体中内皮细胞间连接的下调和内皮含量的降低可能在高胆固醇血症小鼠的勃起功能下降中起主要作用。

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