Korean Journal of Veterinary Research 1997;37(2):311-319.
Relationship between estradiol-17β and IGF-I receptor expression in primary cultured rabbit renal proximal tubule cells
Ho-jae Han, Seong-ahn Nam, Kwon-moo Park
College of Veterinary Medicine, Chonnam National University
초대배양한 신장 근위세뇨관세포에서 estradiol-17β와 IGF-I 수용체 발현과의 상관관계
한호재, 남성안, 박권무
전남대학교 수의과대학, 호르몬연구센터
Abstract
The mechanisms of $estradiol-17{eta}$ 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 $estradiol-17{eta}$on cell growth and IGF-I binding sites using primary cultured renal proximal tubule cells. We have obtained results as follows : $Estradiol-17{eta}(10^{-9})$ has stimulatory effects in cell growth. Cotreatment of $estradiol-17{eta}(10^{-9}M)$ and $IGF-I(5{ imes}10^{-8}M)$ significantly increased the growth of primary rabbit renal proximal tubule cells compared to that of $estradiol-17{eta}$ or 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 $37^{circ}C$ results in higher binding of $^{125}IGF-I$ than that of $23^{circ}C$ or $4^{circ}C$. Maximum binding was observed at $37^{circ}C$ between 30 and 60 minutes. The binding of $^{125}IGF-I$ to both control and $estradiol-17{eta}-treated$ cells was inhibited by unlabelled $IGF-I(10^{-8}{sim}10^{-12}M)$ in a concentration-dependent manner. However, EGF did not compete for $^{125}IGF-I$ binding at $10^{-8}{sim}10^{-12}M$. IGF-I binding to the membranes from both control and $estradiol-17{eta}-treated$ cells was also analyzed. We found that $estradiol-17{eta}-treated$ cells exhibited higher binding activity for IGF-I. When $estradiol-17{eta}$ or tamoxifen alone, or $estradiol-17{eta}$ and tamoxifen cotreated cells were compared, the binding ratio of $^{125}I-IGF-I$ of $estradiol-17{eta}-treated$ cell was significantly increased but was similar to control in both $estradiol-17{eta}$ and tamoxifen cotreated cell. These results suggest that $estradiol-17{eta}$ in part controls cell proliferation by regulating the expression of IGF-I receptors in primary rabbit renal proximal tubule cells.
Key Words: $Estradiol-17{eta}$, IGF-I, Kidney


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