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首页> 外文期刊>FEBS Open Bio >Expression of a urokinase‐type plasminogen activator during tumor growth leads to angiogenesis via galanin activation in tumor‐bearing mice
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Expression of a urokinase‐type plasminogen activator during tumor growth leads to angiogenesis via galanin activation in tumor‐bearing mice

机译：荷瘤小鼠中尿激酶型纤溶酶原激活物的表达通过甘丙肽激活导致血管生成

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Small‐cell lung carcinoma releases progalanin. The released progalanin is activated via a nonclassical processing pathway, being processed into an active form of galanin (1–20) by plasmin in extracellular components. Plasmin is produced from plasminogen activators. To clarify the regulation of progalanin via plasminogen activation by urokinase and tissue‐plasminogen activator (t‐PA), we investigated the regulation mechanism for urokinase and t‐PA expression and their effect on galanin activation. Additionally, we studied the effect of activated galanin on angiogenesis. To determine the effect of cell density, we measured the expression levels of urokinase and t‐PA using real‐time PCR and plasminogen/gelatin zymography in a cell culture. The urokinase expression increased under both high cell density and presence of cell membrane fractions. However, urokinase increments induced by conditioned medium were low. These results indicate that expression of plasminogen activators is regulated by cell membrane factors. We used tumor‐bearing mice to clarify the expression of plasminogen activators and galanin activation. Real‐time PCR showed that urokinase was substantially higher in the central parts of tumors compared to the periphery, and this was confirmed by plasminogen/gelatin zymography. To evaluate the biological effect of plasminogen activators on tumor growth, we used tranexamic acid as a plasminogen inhibitor. Tranexamic acid decreased galanin (1–20) and the hemoglobin content of tumors and suppressed tumor growth. Additionally, galanin had no effect on the hemoglobin content of tumors derived from cells lacking GALR2. These results demonstrate the regulation of urokinase expression in tumors through progalanin activation in extracellular compartments, and confirm that galanin plays a role in angiogenesis.
机译：小细胞肺癌释放普鲁拉宁。释放的普罗拉宁通过非经典的加工途径被激活，被纤溶酶在细胞外成分中加工成甘丙肽的活性形式（1-20）。纤溶酶由纤溶酶原激活剂产生。为了阐明尿素激酶和组织纤溶酶原激活物（t-PA）通过纤溶酶原激活对普鲁拉宁的调节作用，我们研究了尿激酶和t-PA表达的调节机制及其对甘丙肽激活的影响。另外，我们研究了活化的甘丙肽对血管生成的影响。为了确定细胞密度的影响，我们使用实时PCR和纤溶酶原/明胶酶谱法在细胞培养物中测量了尿激酶和t-PA的表达水平。在高细胞密度和细胞膜组分存在下，尿激酶表达增加。但是，条件培养基诱导的尿激酶增加很低。这些结果表明纤溶酶原激活物的表达受到细胞膜因子的调节。我们使用了荷瘤小鼠来阐明纤溶酶原激活剂和甘丙肽激活的表达。实时PCR显示，与周围相比，肿瘤中心部位的尿激酶明显更高，这已被纤溶酶原/明胶酶谱法证实。为了评估纤溶酶原激活物对肿瘤生长的生物学影响，我们使用了氨甲环酸作为纤溶酶原抑制剂。氨甲环酸可降低甘丙肽（1–20）和肿瘤血红蛋白含量，并抑制肿瘤生长。另外，甘丙肽对源自缺乏GALR2的细胞的肿瘤的血红蛋白含量没有影响。这些结果证明了通过细胞外区室中的孕激素的活化来调节肿瘤中尿激酶表达，并证实甘丙肽在血管生成中起作用。

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