Developmental patterns of insulin-like growth factor-I and -II synthesis and regulation in rat fibroblasts
Developmental patterns of insulin-like growth factor-I and -II synthesis and regulation in rat fibroblasts
复制标题
大鼠成纤维细胞中胰岛素样生长因子-I和-II合成和调节的发育模式
作者:
S. O. Adams;S. Nissley;S. Handwerger;M. Rechler
Insulin-like growth factor-I (IGF-I) and IGF-II are chemically similar polypeptides with related receptor specificity and in vitro biological activity1. IGF-I and IGF-II have a 62% amino acid sequence identity and are 38–48% homologous with the A and B domains of human proinsulin. They can be distinguished by specific radioimmunoassays, appear to have different patterns of hormonal regulation, and presumably serve different in vivo biological functions. Plasma IGF-I levels reflect circulating concentrations of pituitary growth hormone (GH), and exogenous IGF-I substitutes for GH in inducing somatic and skeletal growth in GH-deficient rats2. Several recent observations in rats have suggested a possible role for IGF-II in fetal growth. IGF-II levels are 20- to 100-fold higher in fetal rat serum than in maternal serum and decline within days after birth3. IGF-I exhibits the reciprocal developmental pattern—low in the early neonate, rising to adult levels by approximately 4 weeks of age4,5. We recently reported6 that cultured rat embryo fibroblasts synthesize large amounts of multiplication-stimulating activity (MSA or rIGF-II), the rat homologue of human IGF-II7. We now demonstrate that fibroblast cultures established from rats 2 to 50 days of age mimic the developmental switch from IGF-II to IGF-I production observed in serum. In addition, we show that placental lactogen (PL) but not GH stimulates IGF-II synthesis in fetal fibroblasts. By contrast, both GH and PL stimulate IGF-I synthesis in fibroblasts from older rats with no effect on IGF-II synthesis. Stimulation of IGF-II synthesis in fetal fibroblasts by PL provides a mechanism whereby PL may regulate fetal growth.
DOI:
10.1172/jci110001
发表时间:
1981
期刊:
The Journal of clinical investigation
影响因子:
--
作者:
Clemmons,DR;Underwood,LE;VanWyk,JJ
通讯作者:
VanWyk,JJ
影响因子:
6.1
作者:
Hurley,TW;Kuhn,CM;Schanberg,SM;Handwerger,S
通讯作者:
Handwerger,S