Estrogen Affects Development of Alveolar Structures in Whole-Organ Culture of Mouse Mammary Glands

1997 ◽  
Vol 232 (2) ◽  
pp. 340-344 ◽  
Author(s):  
John Barlow ◽  
Theresa Casey ◽  
Jen-Fu Chiu ◽  
Karen Plaut
Keyword(s):  
Organ Culture ◽  
Mammary Glands

scholarly journals Functional Significance of Selective Expression of ERα and ERβ in Mammary Gland Organ Culture

2021 ◽  
Vol 22 (23) ◽  
pp. 13151
Author(s):  
Rajendra G. Mehta
Keyword(s):  
Organ Culture ◽  
Functional Significance ◽  
Precancerous Lesions ◽  
Mammary Glands ◽  
Short Exposure ◽  
Preneoplastic Lesions ◽  
Organ Cultures ◽  
Regulated Gene Expression ◽  
Microarray Analyses ◽  
Map Kinase Pathways

Thoracic pair of mammary glands from steroid hormone-pretreated mice respond to hormones structurally and functionally in organ culture. A short exposure of glands for 24 h to 7,12 Dimethylbenz(a)anthracene (DMBA) during a 24-day culture period induced alveolar or ductal lesions. Methods: To differentiate the functional significance of ERα and ERβ, we employed estrogen receptor (ER) knockout mice. We compared the effects of DMBA on the development of preneoplastic lesions in the glands in the absence of ERα (αERKO) and ERβ (βERKO) using an MMOC protocol. Glands were also subjected to microarray analyses. We showed that estradiol can be replaced by EGF for pretreatment of mice. The carcinogen-induced lesions developed under both steroids and EGF pretreatment protocols. The glands from αERKO did not develop any lesions, whereas in βERKO mice in which ERα is intact, mammary alveolar lesions developed. Comparison of microarrays of control, αERKO and βERKO mice showed that ERα was largely responsible for proliferation and the MAP kinase pathways, whereas ERβ regulated steroid metabolism-related genes. The results indicate that ERα is essential for the development of precancerous lesions. Both subtypes, ERα and Erβ, differentially regulated gene expression in mammary glands in organ cultures.

CORRELATION BETWEEN THE EFFECTS OF HORMONES ON THE SYNTHESIS OF DNA IN EXPLANTS FROM INDUCED RAT MAMMARY TUMOURS AND THE GROWTH OF THE TUMOURS

1974 ◽  
Vol 62 (2) ◽  
pp. 225-240 ◽  
Author(s):  
D. LEWIS ◽  
R. C. HALLOWES
Keyword(s):  
Organ Culture ◽  
Dna Synthesis ◽  
Culture Medium ◽  
Mammary Glands ◽  
Sprague Dawley ◽  
Culture Techniques ◽  
Mammary Tumours ◽  
Sprague Dawley Rats

SUMMARY Explants from 32 mammary tumours induced in Sprague—Dawley rats by 9,10-dimethyl-1,2-benzanthracene (DMBA) were maintained in organ culture for up to 48 h. Insulin, corticosterone, prolactin, growth hormone and oestradiol were added to the culture medium in various combinations and their effects on the DNA synthesis of the explants was studied. DNA synthesis was stimulated by insulin in explants from 30 out of the 32 tumours examined and this group of 30 responsive tumours could be further subdivided. Explants from 16 tumours showed a greater rate of DNA synthesis in medium containing insulin plus corticosterone plus prolactin than in medium containing insulin alone and this higher rate was decreased by oestradiol; this group is referred to as 'prolactin-responsive'. Explants from the remaining 14 tumours did not show a greater rate of DNA synthesis in medium that contained insulin plus corticosterone plus prolactin than in medium containing insulin alone and neither rate was decreased by oestradiol; this group is referred to as 'insulin-responsive'. Explants from two tumours were not stimulated by insulin and these tumours are referred to as 'non-responsive'. After oophorectomy or administration of ergocryptine to tumour-bearing rats, the prolactin-responsive tumours regressed whereas the non-responsive tumours continued to grow. Explants taken from prolactin-responsive tumours 2 weeks after either oophorectomy or administration of ergocryptine were still prolactin-responsive but those taken from insulin-responsive tumours 2 weeks after the same treatment were now also prolactin-responsive. The non-responsive tumours remained non-responsive. The effects of hormones on the DNA synthesis in vitro of explants from growing DMBA-induced tumours were thus different from those on explants of mammary glands from virgin or pregnant Sprague—Dawley rats. It was concluded that it was possible to predict by organ culture techniques the response in vivo of growing mammary tumours to oophorectomy and ergocryptine administration.

Integration of a gene marker into mouse mammary glands during whole organ culture

1995 ◽  
Vol 17 (4) ◽  
pp. 251-256
Author(s):  
Theresa M. Casey ◽  
Karen Plaut
Keyword(s):  
Organ Culture ◽  
Mammary Glands ◽  
Gene Marker

Basal Lamina Formation in DMBA Induced Mammary Carcinoma

1977 ◽  
Vol 35 ◽  
pp. 534-535
Author(s):  
I. Russo ◽  
J. Saby ◽  
J. Russo
Keyword(s):  
Mammary Carcinoma ◽  
Virgin Female ◽  
Mammary Glands ◽  
Sesame Oil ◽  
Female Rats ◽  
Ultrastructural Changes ◽  
Post Inoculation ◽  
Intermediate Type ◽  
Sprague Dawley ◽  
Intercellular Spaces

It has been previously demonstrated that DMBA-induced rat mammary carcinoma originates in the terminal end bud (TEB) of the mammary gland by proliferation of intermediate type cells (1). The earliest lesion identified is the intraductal proliferation (IDP), which gives rise to intraductal carcinomas. These evolve to cribriform, papillary and comedo types (2). In the present work, we report the ultrastructural changes that take place in the IDP for the formation of a cribriform pattern.Fifty-five-day-old Sprague Dawley virgin female rats were inoculated intra- gastrically with 20 mg 7,12-dimethylbenz(a)anthracene (DMBA) in 1 ml sesame oil. Non-inoculated, age-matched females were used as controls. Mammary glands from both control and experimental rats were removed weekly from the time of inoculation until 86 days post-inoculation. The glands were fixed and processed for electron microscopy (2).The first change observed in IDP's was the widening of intercellular spaces and the secretion of an electron dense material into these spaces (Fig. 1).

Freeze-etch observations on the tight junctions of sertoli cells grown in organ culture with FSH

1978 ◽  
Vol 36 (2) ◽  
pp. 340-341
Author(s):  
Rita Meyer ◽  
Zoltan Posalaky ◽  
Dennis Mcginley
Keyword(s):  
Organ Culture ◽  
Tight Junctions ◽  
Sertoli Cell ◽  
Germ Cells ◽  
Sertoli Cells ◽  
Barrier Function ◽  
Cell Junction ◽  
Intramembranous Particles ◽  
Junctional Complexes ◽  
Oriented Parallel

The Sertoli cell tight junctional complexes have been shown to be the most important structural counterpart of the physiological blood-testis barrier. In freeze etch replicas they consist of extensive rows of intramembranous particles which are not only oriented parallel to one another, but to the myoid layer as well. Thus the occluding complex has both an internal and an overall orientation. However, this overall orientation to the myoid layer does not seem to be necessary to its barrier function. The 20 day old rat has extensive parallel tight junctions which are not oriented with respect to the myoid layer, and yet they are inpenetrable by lanthanum. The mechanism(s) for the control of Sertoli cell junction development and orientation has not been established, although such factors as the presence or absence of germ cells, and/or hormones, especially FSH have been implicated.

The effect of bromocriptine on mammary-gland ultrastructure of hyperprolactinemic rats

1984 ◽  
Vol 42 ◽  
pp. 204-205
Author(s):  
I.C. Murray
Keyword(s):  
Mammary Gland ◽  
Dopamine Agonist ◽  
Alveolar Epithelium ◽  
Mammary Glands ◽  
Female Rats ◽  
Control Group ◽  
Cell Hyperplasia ◽  
Once Daily ◽  
Long Evans

In women, hyperprolactinemia is often due to a prolactin (PRL)-secreting adenoma or PRL cell hyperplasia. RRL excess stimulates the mammary glands and causes proliferation of the alveolar epithelium. Bromocriptine, a dopamine agonist, inhibits PRL secretion and is given to women to treat nonpuerperal galactorrhea. Old female rats have been reported to have PRL cell hyperplasia or adenoma leading to PRL hypersecretion and breast stimulation. Herein, we describe the effect of bromocriptine and consequently the reduction in serum PRL levels on the ultrastructure of rat mammary glands.Female Long-Evans rats, 23 months of age, were divided into control and bromocriptine-treated groups. The control animals were injected subcutaneously once daily with a 10% ethanol vehicle and were later divided into a normoprolactinemic control group with serum PRL levels under 30 ng/ml and a hyperprolactinemic control group with serum PRL levels above 30 ng/ml.

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