TY - JOUR
T1 - Regulation of epidermal growth factor receptor by estrogen
AU - Mukku, V. R.
AU - Stancel, G. M.
N1 - Copyright:
Copyright 2004 Elsevier B.V., All rights reserved.
PY - 1985
Y1 - 1985
N2 - Administration of 17β-estradiol (E2) to immature female rats produces a 3-fold increase in 125I-epidermal growth factor (EGF) binding to uterine membranes with no change in the affinity of membrane receptors for EGF. E2 treatment also increases the EGF receptor visualized by sodium dodecyl sulfate-polyacrylamide gel electrophoresis after affinity labeling of uterine membranes and the EGF-stimulated receptor autophosphorylation activity. In addition, E2 administration stimulates EGF-dependent tyrosine kinase activity in an assay system using exogenous angiotensin II as substrate. Following hormone treatment, EGF receptor levels increase between 6 and 12 h, remain elevated at 18 h, and decline between 24 and 36 h. This stimulation of EGF receptor levels by E2 is specific, since the non-estrogenic hormones progesterone, dexamethasone, and dihydrotestosterone fail to elevate receptor levels. E2-stimulated increases in EGF receptor levels are also blocked by cycloheximide and actinomycin D, suggesting that the observed effect represents de novo synthesis of the EGF receptor and may be mediated by a transcriptional mechanism. These results demonstrate that estrogen can regulate acutely the levels of EGF receptor in vivo and raise the possibility that events coupled to this receptor may play a role in estrogen-stimulated growth.
AB - Administration of 17β-estradiol (E2) to immature female rats produces a 3-fold increase in 125I-epidermal growth factor (EGF) binding to uterine membranes with no change in the affinity of membrane receptors for EGF. E2 treatment also increases the EGF receptor visualized by sodium dodecyl sulfate-polyacrylamide gel electrophoresis after affinity labeling of uterine membranes and the EGF-stimulated receptor autophosphorylation activity. In addition, E2 administration stimulates EGF-dependent tyrosine kinase activity in an assay system using exogenous angiotensin II as substrate. Following hormone treatment, EGF receptor levels increase between 6 and 12 h, remain elevated at 18 h, and decline between 24 and 36 h. This stimulation of EGF receptor levels by E2 is specific, since the non-estrogenic hormones progesterone, dexamethasone, and dihydrotestosterone fail to elevate receptor levels. E2-stimulated increases in EGF receptor levels are also blocked by cycloheximide and actinomycin D, suggesting that the observed effect represents de novo synthesis of the EGF receptor and may be mediated by a transcriptional mechanism. These results demonstrate that estrogen can regulate acutely the levels of EGF receptor in vivo and raise the possibility that events coupled to this receptor may play a role in estrogen-stimulated growth.
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M3 - Article
C2 - 2991264
AN - SCOPUS:0022259725
SN - 0021-9258
VL - 260
SP - 9820
EP - 9824
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
IS - 17
ER -