INSULIN-LIKE GROWTH-FACTOR-I STIMULATES AMINO-ACID-UPTAKE BY THE CULTURED HUMAN PLACENTAL TROPHOBLAST

被引:91
作者
KARL, PI
机构
[1] Department of Pediatrics, North Shore University Hospital, Cornell University Medical College, Manhasset, New York
关键词
D O I
10.1002/jcp.1041650111
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Amino acid uptake by the human placenta is known to occur via several transport mechanisms. However, regulation by extracellular factors has received relatively little attention. A recent report by this laboratory characterized the uptake of alpha-aminoisobutyric acid (AIB) stimulated by insulin in the cultured human placental trophoblast. The current study evaluated the effect of insulin-like growth factor-1 (IGF-1) on AIB uptake in cultured human placental trophoblasts. Nai-dependent AIB uptake was significantly stimulated by ICF-I in a time-dependent manner, as early as 30 min after hormone exposure. The maximum effect was at 2-4 hr of continuous exposure to ICF-I and the stimulation was dependent upon IGF-1 concentration approaching maximal stimulation at 50 ng.ml(-1). AIB uptake was inhibited by increasing concentrations of alpha-(methylamino)isobutyric acid (MeAIB). Approximately 75% of basal (unstimulated) Na+-dependent AIB uptake was inhibited by MeAIB. The IGF-l-stimulated increment above basal AIB uptake was completely inhibited by MeAIB. IGF-1 increased the maximum uptake velocity but not Km. Using equimolar concentrations, stimulation was greater with IGF-1 than with IGF-2. Stimulation by IGF-l, but not insulin, was inhibited by anti-ICF-l receptor antibody, indicating mediation via the IGF-1 receptor. H7, a nonspecific inhibitor of serine-threonine kinase, inhibited IGF-1-dependent stimulation of AIB uptake. In addition, calphostin C (a specific inhibitor of protein kinase C), but not H89 (a specific inhibitor of protein kinase A), inhibited the IGF-1 action. This study further characterizes regulated amino acid uptake by the human placental trophoblasts and demonstrates that the Na+-dependent component of AIB uptake is stimulated by physiologic concentrations of IGF-1. (C) 1995 Wiiey-Liss, Inc.
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页码:83 / 88
页数:6
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