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首页> 外文期刊>Molecular urology >Nitric oxide synthase gene therapy for erectile dysfunction: comparison of plasmid, adenovirus, and adenovirus-transduced myoblast vectors.
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Nitric oxide synthase gene therapy for erectile dysfunction: comparison of plasmid, adenovirus, and adenovirus-transduced myoblast vectors.

机译：一氧化氮合酶基因治疗勃起功能障碍：质粒，腺病毒和腺病毒转导的成肌细胞载体的比较。

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BACKGROUND AND PURPOSE: Nitric oxide (NO) has been recognized as an important transmitter for genitourinary tract function. This transmitter mediates smooth muscle relaxation and is essential for erection. The objective of our research was to determine whether overexpression of nitric oxide synthase (NOS) in the corpus cavernosum of the penis would correct erectile dysfunction. MATERIALS AND METHODS: We introduced the inducible form of the enzyme NOS (iNOS) into the corpus cavernosum of adult (250-300 g) male Sprague-Dawley rats by injecting a solution of plasmid, adenovirus, or adenovirus-transduced myoblast cells (adeno-myoblast) (N = 3-5 each group). We also injected plasmid, adenovirus, and adeno-myoblast encoding the expression of the beta-gatactosidase reporter gene. RESULTS: We noted expression of beta-galactosidase throughout the corpora cavernosum after injection of each of the three solutions. Staining was greatest for adeno-myoblast followed by adenovirus and then plasmid. The basal intracavernous pressure (ICP) of iNOS-treated animals (adenovirus and adenovirus-transduced myoblast) increased to 55 +/- 23 cm H(2)O v 5 +/- 6 H(2)O in naive animals (P = 0.001). Stimulation of the cavernous nerve (15 Hz, 1.5 msec, 10-40 V, 1 min) resulted in a twofold increase in ICP (adenovirus and adeno-myoblast) from the basal level of the iNOS-treated animals. Direct in situ measurement of NO demonstrated release of 1 to 1.3 microM NO in the adeno-myoblast-treated penis. CONCLUSION: Myoblast-mediated gene therapy was more successful in delivering iNOS into the corpus cavernosum than were the direct adenovirus or plasmid transfection methods. Gene therapy of NOS may open new avenues of treatment for erectile dysfunction. Control of NOS expression would be necessary to prevent priapism.
机译：背景与目的：一氧化氮（NO）被公认为是泌尿生殖道功能的重要递质。该发射器介导平滑肌松弛，对勃起必不可少。我们研究的目的是确定阴茎海绵体中一氧化氮合酶（NOS）的过度表达是否可以纠正勃起功能障碍。材料和方法：我们通过注射质粒，腺病毒或腺病毒转导的成肌细胞（腺病毒）溶液，将可诱导形式的NOS（iNOS）酶引入成年（250-300 g）雄性Sprague-Dawley大鼠的海绵体中-成肌细胞）（每组N = 3-5）。我们还注射了编码β-半乳糖苷酶报道基因表达的质粒，腺病毒和成肌细胞。结果：我们注意到在注射三种溶液后，整个海绵体中的β-半乳糖苷酶表达。腺成肌细胞染色最大，其次是腺病毒，然后是质粒。 iNOS处理的动物（腺病毒和腺病毒转导的成肌细胞）的基础海绵体腔内压（ICP）增加至幼稚动物中的55 +/- 23 cm H（2）O v 5 +/- 6 H（2）O（P = 0.001）。刺激海绵状神经（15 Hz，1.5毫秒，10-40 V，1分钟）导致ICP（腺病毒和成肌细胞）的含量比经iNOS处理的动物的基础水平增加了两倍。直接原位测量NO可以证明在经成腺细胞处理的阴茎中释放了1至1.3 microM NO。结论：成肌细胞介导的基因治疗比直接腺病毒或质粒转染方法更能成功地将iNOS导入海绵体。 NOS的基因治疗可能为勃起功能障碍开辟新的治疗途径。为了防止阴茎异常勃勃，必须控制NOS表达。

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