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首页> 外文期刊>The journal of sexual medicine >Pentoxifylline attenuates transforming growth factor-beta1-stimulated elastogenesis in human tunica albuginea-derived fibroblasts part 2: Interference in a TGF-beta1/Smad-dependent mechanism and downregulation of AAT1.
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Pentoxifylline attenuates transforming growth factor-beta1-stimulated elastogenesis in human tunica albuginea-derived fibroblasts part 2: Interference in a TGF-beta1/Smad-dependent mechanism and downregulation of AAT1.

机译：己酮可可碱减弱人白膜来源的成纤维细胞中转化生长因子-β1刺激的弹性生成，第2部分：干扰TGF-β1/ Smad依赖性机制和AAT1的下调。

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INTRODUCTION: Transforming growth factor-beta1 (TGF-beta1) contributes to the pathogenesis of Peyronie's disease (PD). Pentoxifylline (PTX) antagonizes the effects of TGF-beta1 and has been utilized in our clinic for the management of PD although the mechanisms of action are not entirely clear. AIM: We studied cell-signaling pathways through which TGF-beta1 and PTX mediate collagen metabolism, elastin expression, and elastogenesis in tunica albuginea-derived fibroblasts (TADFs). METHODS: TADFs from men with and without PD were cultured and treated with TGF-beta1 and PTX as monotherapy at differing concentrations and time points. Combination treatment (TGF-beta1 followed by PTX and vice versa) was also investigated. MAIN OUTCOME MEASURES: Reverse-transcription polymerase chain reaction and Western blotting were utilized to assess differences in elastin metabolism and cellular signaling between groups. Alpha-1 antitrypin (AAT1) expression was assayed. RESULTS: At doses greater than 0.1 ng/Ml, TGF-beta1 increased messenger ribonucleic acid (mRNA) and protein expression of elastin in a time-dependent fashion in TADF. PTX did not interfere with TGF-beta1 mediated upregulation of elastin mRNA and protein in TADF. However, pretreatment of TADF with PTX was associated with decreased expression of AAT1, decreased activity of the Smad1/5 pathway, and enhanced phosphorylation of the inhibitory Smad6. CONCLUSION: Expression of elastin mRNA and protein is upregulated in TADF by TGF-beta1. PTX has no effect on elastin production but attenuates elastogenesis in TADF through an AAT1-related mechanism.
机译：简介：转化生长因子-β1（TGF-β1）促进了佩罗尼氏病（PD）的发病机理。己酮可可碱（PTX）拮抗TGF-β1的作用，尽管其作用机理尚不完全清楚，但已在我们的临床中用于PD的管理。目的：我们研究了细胞信号通路，TGF-beta1和PTX通过该通路介导白膜白膜成纤维细胞（TADFs）中的胶原代谢，弹性蛋白表达和弹性生成。方法：培养患有和不患有PD的男性TADF，并在不同的浓度和时间点分别以TGF-beta1和PTX作为单一疗法进行治疗。还研究了联合治疗（TGF-β1，然后是PTX，反之亦然）。主要观察指标：逆转录聚合酶链反应和蛋白质印迹法用于评估两组之间弹性蛋白代谢和细胞信号传导的差异。分析了Alpha-1抗trypin（AAT1）的表达。结果：在大于0.1 ng / Ml的剂量下，TDF-beta1在TADF中以时间依赖性方式增加了信使核糖核酸（mRNA）和弹性蛋白的蛋白质表达。 PTX不会干扰TDF-beta1介导TADF中弹性蛋白mRNA和蛋白的上调。但是，用PTX预处理TADF与降低AAT1的表达，降低Smad1 / 5途径的活性以及增强抑制性Smad6的磷酸化有关。结论：TGF-β1可上调TADF中弹性蛋白的表达。 PTX对弹性蛋白的产生没有影响，但会通过AAT1相关机制减弱TADF中的弹性生成。

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