Exocrine secretion of epidermal growth factor by the rat prostate: Effect of adrenergic agents, cholinergic agents, and vasoactive intestinal peptide

Jacobs, Stephen C.; Story, Michael T.

doi:10.1002/pros.2990130109

Cited by 36 publications

(14 citation statements)

References 29 publications

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“…Expression of transforming growth factor a (TGFa)/EGF in Sertoli and peritubular cells of the seminiferous tubule is speculated to be involved in the maintenance of testicular function (16). Androgen regulation of EGF and the EGF receptor in rat prostate also suggests that EGF may have an important physiological role (17). Gonadotropin induction of various growth factors (EGF, TGFa, TGF,8, insulin-like growth factor I) in the ovary has been proposed to provide a self-amplification mechanism that perpetuates the gonadotropin signal and thereby allows for fine control of thecal and granulosa cell growth and differentiation (18).…”

Section: Discussionmentioning

confidence: 99%

Epidermal growth factor replaces estrogen in the stimulation of female genital-tract growth and differentiation.

Nelson

Takahashi

Bossert

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

359

167

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The in vivo studies presented here demonstrate that epidermal growth factor (EGF) is an important autocrine and/or paracrine mediator of estrogen-induced growth and differentiation in mouse uterus and vagina. An antibody specific for EGF significantly inhibited estrogeninduced uterine and vaginal growth, thereby implicating EGF involvement in estrogen action. Furthermore, EGF administered via slow-release pellets in ovariectomized mice acted as a potent uterine and vaginal mitogen as well as an inducer of vaginal keratinization. Experiments with ovariectomized, adrenalectomized, hypophysectomized mice indicated that EGF mitogenesis does not require pituitary or adrenal hormones. Treatment with EGF also mimicked estrogen in the induction of uterine lactoferrin (a major estrogen-inducible secretory protein) mRNA and protein. These data suggest that EGF has estrogen-like effects in the promotion of cell growth in the reproductive tract and that EGF may serve as an important mediator of estrogen action in vivo.Estrogen-induced growth of various target tissues is mediated, in part, by the production of polypeptide growth factors, which may act in an autocrine or paracrine fashion to stimulate proliferation (1, 2). Two polypeptide growth factors, insulin-like growth factor I and epidermal growth factor (EGF), have been associated with the induction of uterine growth by estrogen (2, 3). Our laboratory and others have demonstrated that immunoreactive EGF precursor is present in the mouse uterus (3, 4), that estrogen treatment enhances the expression of EGF (3, 4) and EGF receptor (5) in the uterus, and that EGF is a potent mitogen in mouse uterine cell cultures (6). These studies provide evidence suggesting that EGF plays an important role in estrogen-induced uterine growth.Previous studies (3, 6) suggesting that EGF plays a role in uterine growth led us to further evaluate the role of EGF as a potential regulator of reproductive-tract growth in vivo. In this study, we demonstrate that estrogen action is inhibited by an EGF-specific antibody and that in vivo exposure to EGF alone mimics estrogen in the induction of uterine and vaginal growth and differentiation. Our results strongly suggest that EGF acts as an estrogen-inducible physiological mediator of mouse reproductive-tract growth in vivo. MATERIALS AND METHODS Quantitation of Uterine and Vaginal Growth FollowingExposure to an EGF-Specific Antibody. To determine whether an antibody specific for EGF could inhibit estrogen-induced growth, slow-release cholesterol-based pellets containing an antibody against EGF (whole antiserum; 2.5 mg per pellet; Collaborative Research) were prepared by Innovative Research of America. These pellets were divided into fourths and one quarter was implanted under the kidney capsule of 8-week-old female CD-1 mice that had been ovariectomized for at least 3 weeks. Appropriate control pellets containing normal whole serum (rabbit; 2.9 mg per pellet; Calbiochem) were also implanted. Three days following pellet implantation, the anim...

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Section: Discussionmentioning

confidence: 99%

Epidermal growth factor replaces estrogen in the stimulation of female genital-tract growth and differentiation.

Nelson

Takahashi

Bossert

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

359

167

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“…In the rat prostate, catecholamines have been shown to involve both growth and expression of specific proteins, an effect mediated bya-adrenergic receptors. Catecholamines can function as mitogens in several target tissues, including the prostate gland, acting directly through the adrenergic receptors or through receptor-mediated induction of other growth factors, such as epithelial growth factor (EGF) [23].…”

Section: Role Of Adrenergic Agonists and Antagonists In Prostate Tissuementioning

confidence: 99%

Prostate innervation

McVary¹,

McKenna²,

Lee³

1998

Prostate

111

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“…In rat ventral prostate, EGF was detected and shown to be regulated by androgen (13,16,17,30). TGF-␣ is structurally and biochemically similar to EGF.…”

Section: Discussionmentioning

confidence: 97%

“…TGF-␣ is structurally and biologically similar to EGF. High concentrations of EGF were determined in rat prostate (16,17). EGFR expression was observed in rat epithelial cells (18).…”

mentioning

confidence: 99%

Developmental and Hormonal Regulation of Transforming Growth Factor-α and Epidermal Growth Factor Receptor Gene Expression in Isolated Prostatic Epithelial and Stromal Cells*

1998

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Androgen has an important role in development of the prostate, and the actions of androgen are mediated, in part, by locally produced growth factors. These growth factors are postulated to mediate stromal-epithelial interaction in the prostate to maintain normal tissue physiology. Transforming growth factor-␣ (TGF-␣) is one of the growth factors that can stimulate prostatic growth. The expression of TGF-␣ is thought to be regulated by androgen. The expression of epidermal growth factor receptor (EGFR), which is the receptor of TGF-␣ and EGF, also may be regulated by androgen. The hormonal and developmental regulation of TGF-␣ and EGFR messenger RNA (mRNA) levels in isolated epithelial and stromal cells from rat ventral prostate was investigated. The expression of mRNA for TGF-␣ and EGFR was analyzed by a quantitative RT-PCR (QRT-PCR) procedure developed. Observations from this assay demonstrated that both epithelial and stromal cells expressed the mRNA for TGF-␣ and EGFR. TGF-␣ mRNA expression was constant during postnatal, pubertal, and adult development of the prostate. EGFR mRNA expression was elevated at the midpubertal period and decreased with age. After castration of 60-day-old adult rats, both TGF-␣ and EGFR mRNA were significantly enhanced. TGF-␣ mRNA expression was stimulated by EGF in stromal cells (4.5-fold increase) but was not changed by any treatment in epithelial cells. EGFR mRNA levels were stimulated by EGF and keratinocyte growth factor treatment and inhibited by testosterone treatment in epithelial cells. Stromal cell EGFR mRNA levels were not affected by any treatment. Both testosterone and EGF stimulated incorporation of 3 H-thymidine into prostatic stromal and epithelial cells. Anti-TGF-␣ antibody significantly inhibited testosterone-stimulated Results indicate that testosterone does not directly regulate TGF-␣ mRNA levels but does inhibit EGFR mRNA levels. Interestingly, anti TGF-␣ antibody suppressed the effect of testosterone on 3 H-thymidine incorporation into prostatic stromal and epithelial cells. This finding suggests that testosterone may act indirectly on prostatic cells to influence TGF-␣ actions. TGF-␣ mRNA levels were influenced by EGF in stromal cells only, and EGFR mRNA levels were influenced by testosterone, EGF, and keratinocyte growth factor in epithelial cells. These observations suggest that regulation of TGF-␣ and EGFR is distinct between the cell types. In conclusion, a network of hormonally controlled growth factor-mediated stromal-epithelial interactions is needed to maintain prostate development and function. (Endocrinology 139: 1369 -1377, 1998)

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Exocrine secretion of epidermal growth factor by the rat prostate: Effect of adrenergic agents, cholinergic agents, and vasoactive intestinal peptide

Cited by 36 publications

References 29 publications

Epidermal growth factor replaces estrogen in the stimulation of female genital-tract growth and differentiation.

Epidermal growth factor replaces estrogen in the stimulation of female genital-tract growth and differentiation.

Prostate innervation

Developmental and Hormonal Regulation of Transforming Growth Factor-α and Epidermal Growth Factor Receptor Gene Expression in Isolated Prostatic Epithelial and Stromal Cells*

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