Stimulating effect of both human recombinant inhibin A and activin A on immature porcine Leydig cell functions in vitro.
Stimulating effect of both human recombinant inhibin A and activin A on immature porcine Leydig cell functions in vitro.
复制标题
人重组抑制素 A 和激活素 A 对未成熟猪 Leydig 细胞功能的体外刺激作用。
作者：
H. Lejeune;F. Chuzel;P. Sanchez;P. Durand;J. Mather;J. Saez
除了调节 FSH 分泌外，已经清楚地表明抑制素和激活素在性腺中具有旁分泌/自分泌作用。我们在体外研究了人重组抑制素A和人重组激活素A对未成熟猪Leydig细胞的影响。 Leydig 细胞通过胶原酶消化 3 周龄仔猪的睾丸来制备，在 Percoll 梯度上纯化，然后在化学成分确定的培养基中培养。用增加量的抑制素A或激活素A(0.5-200ng/ml)处理细胞。在 Leydig 细胞上直接应用抑制素 A 或激活素 A 4 或 48 小时不会刺激基础睾酮分泌。相反，用任一因子处理细胞48小时都会导致hCG刺激的睾酮分泌呈剂量依赖性增加（10[-9] M hCG，2小时），抑制素A和激活素A的最大效果分别增加2.40 +/- 0.37倍和2.43 +/- 0.37倍，并且这些变化与LH/hCG结合位点的轻微增加有关。 （增加 1.37 +/- 0.19 和 1.24 +/- 0.11 倍）。此外，抑制素 A 和激活素 A 均增强 LH/hCG 受体的信使 RNA (mRNA) 水平（增加 2.75 +/- 0.40 和 2.53 +/- 0.60 倍）和细胞色素 P450 17α-羟化酶（增加 6 +/- 1 和 3.5 +/- 0.6 倍），但对侧链裂解细胞色素没有影响 P450 或细胞色素 P450 芳香酶 mRNA。激活素 A 使 3β-羟基类固醇脱氢酶 mRNA 水平增加（增加 3.1 +/- 1.3 倍），但抑制素 A 则不然。然而，抑制素 A 阻断了激活素 A 的刺激作用。与类固醇生成酶 mRNA 的这些变化一致，两种肽都增强了外源 22R-羟基胆固醇和黄体酮的转化，但只有激活素 A 增加 脱氢表雄酮转化为睾酮。总之，我们的研究结果表明，抑制素 A 和激活素 A 对未成熟猪 Leydig 细胞的体外分化功能具有刺激作用。由于抑制素对体外大鼠间质细胞功能具有刺激作用而激活素具有抑制作用，因此这些因素对间质细胞的影响似乎具有物种依赖性。
In addition to the regulation of FSH secretion, it has been clearly shown that inhibin and activin have paracrine/autocrine effects in the gonads. We have studied the effect of human recombinant inhibin A and human recombinant activin A on immature porcine Leydig cells in vitro. Leydig cells were prepared by collagenase digestion of testes from 3-week-old piglets, purified on Percoll gradient, then cultured in a chemically defined medium. The cells were treated with increasing amounts of inhibin A or activin A (0.5-200 ng/ml). Direct application of either inhibin A or activin A on Leydig cells for 4 or 48 h did not stimulate basal testosterone secretion. Conversely, treatment of the cells for 48 h with either factor resulted in a dose-dependent increase in hCG-stimulated testosterone secretion (10[-9] M hCG, 2 h) with a maximal effect of 2.40 +/- 0.37- and 2.43 +/- 0.37-fold increases for inhibin A and activin A, respectively, and these changes were associated with a slight increase in LH/hCG-binding sites (1.37 +/- 0.19- and 1.24 +/- 0.11-fold increases). In addition, both inhibin A and activin A enhanced messenger RNA (mRNA) levels of LH/hCG receptor (2.75 +/- 0.40- and 2.53 +/- 0.60-fold increases) and cytochrome P450 17alpha-hydroxylase (6 +/- 1- and 3.5 +/- 0.6-fold increases), but had no effect on side-chain cleavage cytochrome P450 or cytochrome P450 aromatase mRNAs. 3beta-Hydroxysteroid dehydrogenase mRNA levels were increased (3.1 +/- 1.3-fold increase) by activin A, but not by inhibin A. However, inhibin A blocked the stimulatory action of activin A. In keeping with these changes in the steroidogenic enzyme mRNAs, both peptides enhanced the conversion of exogenous 22R-hydroxycholesterol and progesterone, but only activin A increased the conversion of dehydroepiandrosterone into testosterone. In conclusion, our findings demonstrate that both inhibin A and activin A have a stimulatory effect on immature porcine Leydig cell differentiated function in vitro. As inhibin has a stimulatory and activin has an inhibitory effect on rat Leydig cell function in vitro, the effects of these factors on Leydig cells seem to be species dependent.
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DOI：
10.1073/pnas.91.19.8817
发表时间：
1994-09-13
影响因子：
11.1
作者：
MATZUK, MM;FINEGOLD, MJ;BRADLEY, A
通讯作者：
BRADLEY, A
大鼠睾丸细胞类型中抑制素亚基的差异产生和调节。
影响因子：
4.8
作者：
Roberts,V;Meunier,H;Sawchenko,PE;Vale,W
通讯作者：
Vale,W
牛肾上腺皮质细胞色素 P-450(17 α)。
DOI：
--
发表时间：
1986
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Zuber,MX;John,ME;Okamura,T;Simpson,ER;Waterman,MR
通讯作者：
Waterman,MR
研究抑制素和激活素在生殖、肿瘤发生和发育中的作用的转基因模型。
DOI：
--
发表时间：
1996
期刊：
Recent progress in hormone research.
影响因子：
--
作者：
Matzuk,MM;Kumar,TR;Shou,W;Coerver,KA;Lau,AL;Behringer,RR;Finegold,MJ
通讯作者：
Finegold,MJ
通过 II 型激活素受体的激活素信号传导会导致抑制素缺陷小鼠出现恶病质样症状。
DOI：
10.1210/mend.10.5.8732684
发表时间：
1996
期刊：
Molecular endocrinology (Baltimore, Md.)
影响因子：
--
作者：
Coerver,KA;Woodruff,TK;Finegold,MJ;Mather,J;Bradley,A;Matzuk,MM
通讯作者：
Matzuk,MM