Vasopressin stimulates growth of renal epithelial cells in culture.
Vasopressin stimulates growth of renal epithelial cells in culture.
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加压素刺激培养物中肾上皮细胞的生长。
DOI：
10.1152/ajpcell.1983.245.5.c365
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发表时间：
1983
期刊：
影响因子：
--
通讯作者：
Toback,FG
中科院分区：
文献类型：
--
作者：
Walsh-Reitz,MM;Toback,FG
在BSC-1细胞系培养中，研究了精氨酸抗利尿素通过影响Na+转运来调节肾上皮细胞生长的假设。在培养基中加入抗利尿激素（75 pg/ml）或NaCl （25 mM）可以刺激融合培养的生长，但在0.5%小牛血清的存在下，会阻碍稀疏细胞的生长。因此，抗利尿激素或外源NaCl调节BSC-1细胞生长的能力是细胞密度依赖性的。加压素仅在50-100 pg/ml（约10(-10)M）的狭窄浓度范围内刺激融合培养物的生长，而10 pg/ml和125-1,000 pg/ml的浓度则没有影响。而加压素在10 pg/ml及以上浓度时，可使细胞内Na+含量达到最大值，说明加压素可以在不刺激细胞生长的情况下提高细胞内Na+含量。为了确定抗利尿激素是否通过作用于质膜来调节生长，在高密度静止培养中评估了营养转运和配体结合。激素增加了α -氨基异丁酸的吸收和表皮生长因子的结合，而NaCl （25 mM）的添加则没有作用。因此，抗利尿激素的生长刺激与细胞Na+含量增加、氨基酸摄取增强和生长因子结合增强有关。这些观察结果表明，抗利尿激素的促生长作用不是其改变细胞Na+通量的能力的简单功能，而是可能由激素的其他作用介导，可能在质膜水平上。
The hypothesis that arginine vasopressin could regulate kidney epithelial growth by its effect on Na+ transport was examined in cultures of cells from the BSC-1 line. Addition of vasopressin (75 pg/ml) or NaCl (25 mM) to the medium stimulated growth of confluent cultures but retarded growth of sparse cells in the presence of 0.5% calf serum. Thus the capacity of vasopressin or exogenous NaCl to regulate growth of BSC-1 cells was cell density dependent. Vasopressin stimulated growth of confluent cultures only in the narrow concentration range of 50-100 pg/ml (approximately 10(-10)M), whereas concentrations of 10 pg/ml and 125-1,000 pg/ml had no effect. In contrast, vasopressin at or above concentrations of 10 pg/ml raised cell Na+ content to its maximal value, which indicated that the hormone could increase the Na+ content of cells without necessarily stimulating their growth. To determine if vasopressin modulates growth by acting on the plasma membrane, nutrient transport and ligand binding were assessed in high-density quiescent cultures. The hormone augmented uptake of alpha-aminoisobutyric acid and binding of epidermal growth factor, whereas the addition of NaCl (25 mM) did not. Thus growth stimulation by vasopressin was associated with increased cell Na+ content, enhanced uptake of an amino acid, and augmented binding of a growth factor. These observations suggest that the growth-promoting effect of vasopressin is not a simple function of its capacity to alter cell Na+ flux but could be mediated by other actions of the hormone, perhaps at the level of the plasma membrane.