EGF receptor regulation in normal mouse mammary gland.
EGF receptor regulation in normal mouse mammary gland.
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正常小鼠乳腺中 EGF 受体的调节。
DOI：
10.1002/jcp.1041520315
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发表时间：
1992
影响因子：
5.6
通讯作者：
Nummy,KA
中科院分区：
文献类型：
--
作者：
Haslam,SZ;Counterman,LJ;Nummy,KA
已知雌激素（E）、孕酮（P）和表皮生长因子（EGF）调节正常乳腺的生长和发育，并且EGF可能与E和/或P相互作用。已在乳腺上皮细胞和基质细胞中检测到雌激素（ER）、孕酮（PR）和EGF受体（EGF-R），各种细胞类型在激素依赖性生长调节中的相对作用尚不清楚。本研究旨在确定E和/或P是否通过对EGF-R水平产生调节作用来影响EGF作用，以及哪些细胞类型受到影响。在未成熟的、青春期5周龄和性成熟的10周龄雌性小鼠中检查了卵巢切除术和激素治疗对EGF-R水平的比较作用。EGF-R被表征为单一类别的高亲和力位点，并且在5周龄小鼠的腺体中，EGF-R浓度高出2倍。卵巢切除术对两个年龄组的EGF-R浓度没有显著影响，E和/或P治疗对5周龄小鼠上皮细胞或基质细胞中的EGF-R水平没有影响。相比之下，E+P处理导致10周龄小鼠乳腺上皮中受体浓度增加2倍。因此，腺体的发育状态似乎可以决定EGF、E和P相互作用的性质和程度。© 1992 Wiley利斯公司。
Estrogen (E), progesterone (P), and epidermal growth factor (EGF) are known to regulate growth and development of the normal mammary gland, and it is possible that EGF may interact with E and/or P. Estrogen (ER), progesterone (PR), and EGF receptors (EGF‐R) have been detected in both mammary epithelial and stromal cells, and the relative roles of the various cells types in hormone‐dependent growth regulation are not known. The present studies were undertaken to determine if E and/or P influence EGF action by exerting a regulatory effect on EGF‐R levels and which cell types are affected. The comparative effects of ovariectomy and hormone treatments on EGF‐R levels were examined in immature, pubertal 5‐week‐old and sexually mature 10‐week‐old female mice. EGF‐R were characterized as a single class of high affinity sites and EGF‐R concentration was 2‐fold higher in glands of 5‐week‐old mice. Ovariectomy had no significant effect on EGF‐R concentration in either age group, and treatment with E and/or P had no effect on EGF‐R levels in either epithelial or stromal cells in 5‐week‐old mice. In contrast, E+P treatment caused a 2‐fold increase in receptor concentration in 10‐week‐old mice in the mammary epithelium. Thus it appears that the developmental state of the gland may determine the nature and extent of the interaction of EGF, E, and P. © 1992 Wiley‐Liss, Inc.