Animal model of uterine adenomyosis: Is prolactin a potent inducer of adenomyosis in mice?

Mori, Taketoshi; Singtripop, Tippawan; Kawashima, Seiichiro

doi:10.1016/0002-9378(91)90258-s

Cited by 54 publications

(34 citation statements)

References 22 publications

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“…One experimental model involved transplant of the anterior pituitary in the lumen of adult SHN and SLN mouse strains (Mori & Nagasawa 1983, Mori et al 1991. Almost all animals developed adenomyosis in both uterine horns.…”

Section: Introductionmentioning

confidence: 99%

The effects of tamoxifen and estradiol on myometrial differentiation and organization during early uterine development in the CD1 mouse

Mehasseb

Bell²,

Habiba³

2009

Reproduction

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We used a neonatal mouse model to examine the histogenesis of uterine adenomyosis, and to test whether adenomyosis is due to an abnormality in myometrial differentiation, or in extracellular matrix proteins expression. We also studied the effects of tamoxifen and estradiol on uterine development, myometrial differentiation, and organization. Female CD1 pups were treated with oral tamoxifen (1 mg/kg) (nZ27) or estradiol (0.1 mg/kg) (nZ24) from age 1 to 5 days. Uteri from control (nZ27) and treated mice were obtained on days 2, 5, 10, 15, and 42 of age. We examined the sections histologically, using image analysis and immunohistochemistry for a-smooth muscle actin (a-SMA), desmin, vimentin, laminin, fibronectin, and estrogen receptor-a. Following tamoxifen exposure, all uteri showed adenomyosis by 6 weeks of age (seen as early as day 10). The inner myometrium showed thinning, lack of continuity, disorganization, and bundling. a-SMA expression was normal. Desmin expression normally showed a wave of maturation that was absent in tamoxifen-treated mice. In the estradiol group, adenomyosis was not observed. All uterine layers were normally developed, but hypertrophied. The inner myometrium retained its circular arrangement. There was no difference in the localization of laminin or fibronectin between groups (laminin expression was reduced in the tamoxifen treated uteri). Vimentin could not be detected in all groups. Our results suggest that the development of the inner myometrium is particularly sensitive to estrogen antagonism, and can be affected by steroid receptors modulation. Disruption of the inner myometrium may play a role in the development of uterine adenomyosis.

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Section: Introductionmentioning

confidence: 99%

The effects of tamoxifen and estradiol on myometrial differentiation and organization during early uterine development in the CD1 mouse

Mehasseb

Bell²,

Habiba³

2009

Reproduction

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“…We have established that ectopic pituitary isografts induced uterine adenomyosis in mice associated with hyperprolactinemia [3,5,6]. The early morphological disorder of adenomyosis development is an infiltration of the endometrial stromal cells into the inner myometrium.…”

Section: Discussionmentioning

confidence: 99%

“…This lesion which is also considered to be one of the causes of sterility has attracted much attention for a long time [7,11]. We found that ectopic pituitary isografts induced an early and high incidence of uterine adenomyosis in mice associated with hyperprolactinemia, and suggested that prolactin plays an important role in the genesis of adenomyosis [3,5,6].…”

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confidence: 95%

Histochemical Analysis Using Lectin in the Mouse Uterine Tissues with Experimentally-Induced Adenomyosis.

Sasabe

Matsuda

Mori

1998

Acta Histochem. Cytochem

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“…On the other hand, PRL receptors, especially long-form ones (PRLR-L) [19], are present in the uteri of rats. PRL is known to play important roles in adenomyosis formation in Swiss mice [20][21][22].Bromocriptine (BRC), a dopamine agonist, inhibits inverted growth of the uterine epithelium to the muscle layer in the uterine cervix in ovarietomized mice treated with E2 and PRL [23]. These reports indicate that direct action of PRL on the uterus should be considered as one factor related to uterine carcinogenicity in rats.…”

mentioning

confidence: 99%

“…The effects of PRL and BRC on the uterine proliferating lesions in the uteri of mice are controversial [23]. Mori et al reported that an increase in the plasma level of PRL induces adenomyosis in mice through increased expression of PRL receptor mRNA in the uterus [20][21][22]. On the other hand, BRC-treatment for 30 days induces proliferation of endometrial epithelial cells in mice [37].…”

mentioning

confidence: 99%

Long-Term Treatment with Bromocriptine Inhibits Endometrial Adenocarcinoma Development in Rats

Yoshida

Watanabe

Suzuki

et al. 2009

Journal of Reproduction and Development

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Abstract. The effects of long-term blockade of prolactin (PRL) action by bromocriptine (BRC) treatment on uterine carcinogenesis and on related ovarian physiology were investigated using a rat uterine cancer model. Ten-week-old cycling female Donryu rats, a high yield strain for uterine corpus tumors (endometrial adenocarcinomas), were treated with N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG), as a tumor initiator, and injected with 1 mg/kg body weight BRC subcutaneously 4 times per week until 14.5 months of age to block the proestrus PRL surge. The study was terminated at 15 months of age, and the results showed that long-term BRC treatment significantly inhibited endometrial adenocarcinoma development in terms of both incidence (34.6% to 13.0% with significant difference at 5%) and multiplicity (0.35 to 0.18 with significant difference at 5%), which indicates the number of adenocarcinomas per animals. While BRC did not affect estrous cyclicity in the treated animals, a significant decline was evident in the serum 17β-estradiol (E2) to progesterone (P) ratio (E: P ratio), and the serum E2 level showed a decreased tendency at 15 months of age. While the precise pathway to the inhibitory effect could not be determined; the pathway by which ovarian hormonal imbalance decreases the serum E: P ratio most likely plays a crucial role. Key words: Bromocripchne, Long-term treatment, Prolactin blockade, Rat, Uteirne carcinogenesis (J. Reprod. Dev. 55: [105][106][107][108][109] 2009) varian steroidhormone imbalance contributes to uterine carcinogenesis in human beings [1]. Maekawa et al. [2][3][4] have provided evidence that a similar imbalance, especially elevated 17β-estradiol (E2) levels relative to progesterone (P) levels (the E:P ratio), plays a crucial role in promoting endometrial adenocarcinoma development in rodents. While it is well-established that E2 and estrogenic chemicals play supportive or sometimes initiative roles in uterine carcinogenesis in rats as well as women, P may exert an inhibitory influence on human uterine cancer development [5][6][7]. However, the effects of other hormones related to the pituitary or ovaries on uterine carcinogenesis are not well known.Prolactin (PRL) is one of the important regulators of the corpus luteum as well as luteinizing hormone (LH), prostaglandin and vascular endothelial growth factors and platelet derived growth factors in rats [8][9][10]. The function of PRL as a luteotrophic and luteolytic hormone, however, is very complex [11][12][13][14][15][16][17]. Repeated injection of PRL has been shown to stimulate rapid regression of the persistent corpus luteum, with a concomitant decline in total steroidogenic capacity [12,18]. These studies indicate the possibility that the modulation of P production induced by PRL or its inhibitor affect uterine carcinogenesis through ovarian hormonal imbalance. On the other hand, PRL receptors, especially long-form ones (PRLR-L) [19], are present in the uteri of rats. PRL is known to play important roles in adenomyosis formation in ...

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Animal model of uterine adenomyosis: Is prolactin a potent inducer of adenomyosis in mice?

Cited by 54 publications

References 22 publications

The effects of tamoxifen and estradiol on myometrial differentiation and organization during early uterine development in the CD1 mouse

The effects of tamoxifen and estradiol on myometrial differentiation and organization during early uterine development in the CD1 mouse

Histochemical Analysis Using Lectin in the Mouse Uterine Tissues with Experimentally-Induced Adenomyosis.

Long-Term Treatment with Bromocriptine Inhibits Endometrial Adenocarcinoma Development in Rats

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