NITRIC-OXIDE SYNTHASE (NOS-I) IN LEYDIG-CELLS OF THE HUMAN TESTIS

NITRIC-OXIDE SYNTHASE (NOS-I) IN LEYDIG-CELLS OF THE HUMAN TESTIS
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DOI:
10.1679/aohc.58.17
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发表时间:
1995-03-01
影响因子:
--
通讯作者:
HOLSTEIN, AF
HOLSTEIN, AF
中科院分区:
其他
文献类型:
--
作者:
DAVIDOFF, MS;MIDDENDORFF, R;HOLSTEIN, AF

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用免疫细胞化学方法,在人睾丸的许多Leydig细胞以及MA-10肿瘤和TM 3非肿瘤小鼠Leydig细胞系中,识别了脑型一氧化氮合酶(NOS-I)的免疫反应性。免疫细胞化学结果表明,在Leydig细胞胞质中存在已知激活NOS-I的因子,如谷氨酸和天冬氨酸,以及参与NOS-I活性调节的分子,如钙调蛋白和C2+/钙调蛋白依赖性蛋白激酶II。睾丸间质细胞、支持细胞、部分睾丸内皮细胞、MA-10-和TM-3小鼠间质细胞也显示较强的NADPH-黄递酶活性。双序贯免疫染色提供的证据表明,睾丸Leydig细胞的NOS样免疫反应性与睾酮、钙调蛋白、天冬氨酸、谷氨酸和Ca 2 +/钙调蛋白依赖性蛋白激酶II共定位。硝普钠处理没有导致MA-10-或TM 3小鼠Leydig细胞cGMP形成增加,表明这些细胞产生的NO主要以旁分泌方式起作用,NOS-Ⅰ免疫反应阳性的Leydig细胞产生的NO可作为信使:(1)在相邻的NOS-Ⅰ阳性和/或阴性Leydig细胞之间传递信息,并介导细胞内外多种神经活性物质和生长因子的作用;(3)间质细胞与管周肌成纤维细胞之间的相互作用,影响其收缩和固有层的通透性。
By means of immunocytochemical methods, immunoreactivity for the brain isoform of nitric oxide synthase (NOS-I) was recognized in numerous Leydig cells of the human testis as well as in MA-10 tumor and TM3 non-tumor mouse Leydig cell lines, Within the Leydig cell cytoplasm, immunocytochemical results suggested the occurrence of factors known to activate NOS-I such as glutamate and aspartate, as well as molecules involved in the regulation of the NOS-I activity such as calmodulin and C2+/calmodulin-dependent protein kinase II. Leydig cells, Sertoli cells, some endothelial cells of the testis, MA-10- and TM3 mouse Leydig cell lines exhibited a relatively strong NADPH-diaphorase enzyme activity as well. Double sequential immunostainings provided evidence that NOS-like immunoreactivity of the testicular Leydig cells is colocalized with testosterone, calmodulin, aspartate, glutamate, and Ca2+/calmodulin-dependent protein kinase II, Sodium nitroprusside treatment did not result in increased cGMP formation by MA-10- or TM3 mouse Leydig cells, suggesting that NO produced by these cells acts primarily in a paracrine fashion,The NO produced by NOS-I immunoreactive Leydig cells may act as a messenger: 1) between neighbouring NOS-I positive and/or negative Leydig cells as well as to mediate the action of numerous intracellular and extracellular neuroactive substances and growth factors; 2) between Leydig cells and the muscle cells or pericytes of blood vessels to regulate local blood flow and permeability; and 3) between Leydig cells and peritubular myofibroblasts to influence their contraction and the permeability of the lamina propria.