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KMID : 0359319970370020311
Korean Journal of Veterinary Research
1997 Volume.37 No. 2 p.311 ~ p.319
Relationship between estradiol-17¥â and IGF-I receptor expression in primary cultured rabbit renal proximal tubule cells



Abstract
The mechanisms of estradiol-17¥â regulating growth of both normal and neoplastic cells are not clear until now. In studies using various estrogen-dependent breast cell lines, it is recently known that estrogen controls the cell growth by regulating the expression of growth factors and/or their receptors. In the present study, we investigated the effects of estradiol-17¥âon cell growth and IGF-I binding sites using primary cultured renal proximal tubule cells. We have obtained results as follows :
Estradiol-17¥â(10^(-9)M) has stimulatory effects in cell growth. Cotreatment of estradiol-17¥â(10^(-9)M) and IGF-I(5 x 10^(-8)M) significantly increased the growth of primary rabbit renal proximal tubule cells compared to that of estradiol-17¥âor IGF-I alone treated cells. In binding studies, we found that the binding of ^(125)IGF-I on cell membranes was incubation time- and temperature-dependent. Incubation at 37¡É results in higher binding of ^(125)IGF-I than that of 23¡É or 4 ¡É. Maximum binding was observed at 37¡É between 30 and 60 minutes. The binding of ^(125)IGF-I to both control and estradiol-l7¥â-treated cells was inhibited by unlabelled IGF-I(10^(-8)¡­10^(-12)M) in a concentration-dependent manner. However, EGF did not compete for ^(125)IGF-I binding at 10^(-8)¡­10^(-12)M. IGF-I binding to the membranes from both control and estradiol-l7¥â-treated cells was also analyzed. We found that estradiol-l7¥â-treated cells exhibited higher binding activity for IGF-I. When estradiol-17¥âor tamoxifen alone, or estradiol-17¥âand tamoxifen cotreated cells were compared, the binding ratio of ^(125)I-IGF-I of estradiol-l7¥â-treated cell was significantly increased but was similar to control in both estradiol-17¥âand tamoxifen cotreated cell.
These results suggest that estradiol-l7¥âin part controls cell proliferation by regulating the expression of IGF-I receptors in primary rabbit renal proximal tubule cells.
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