Ultrastructural Changes in the Mammary Epithelial Cell Population During Neoplastic Development Induced by A Chemical Carcinogen.

1976 ◽  
Vol 34 ◽  
pp. 250-251 ◽  
Author(s):  
J. Russo ◽  
W. Isenberg ◽  
M. Ireland ◽  
I.H. Russo
Keyword(s):  
Mammary Gland ◽  
Cell Population ◽  
Virgin Female ◽  
Histological Change ◽  
Mammary Epithelial ◽  
Female Rats ◽  
Ultrastructural Changes ◽  
Post Inoculation ◽  
Chemical Carcinogen ◽  
Sprague Dawley

The induction of rat mammary carcinoma by the chemical carcinogen DMBA is used as a model for the study of the human disease (1). We previously described the histochemical changes that occur in the mammary gland of DMBA treated animals before the earliest manifested histological change, the intraductal proliferation (IDP), was observed (2). In the present work, we demonstrate that a change in the stable cell population found in the resting mammary gland occurs after carcinogen administration.Fifty-five day old Sprague-Dawley virgin female rats were inoculated intragastrically with 20mg of 7,12-dimethylbenz(a)anthracene (DMBA) in 1ml sesame oil. Non-inoculated, age-matched females were used as controls. Mammary glands from control and inoculated rats were removed weekly from the time of inoculation until 60 days post-inoculation. For electron microscopy, the glands were immersed in Karnovsky's fixative, post-fixed in 1% OsO4, dehydrated, and embedded in an Epon-Araldite mixture. Thick (lμ) sections were stained with 1% toluidine blue and were used for selecting areas for ultrastructural study.

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).

Ultrastructural Description of three Different Epithelial Cell Types in Rat Mammary Gland.

1976 ◽  
Vol 34 ◽  
pp. 146-147
Author(s):  
I.H. Russo ◽  
M. Ireland ◽  
W. Isenberg ◽  
J. Russo
Keyword(s):  
Mammary Gland ◽  
Virgin Female ◽  
Cell Types ◽  
Myoepithelial Cells ◽  
Uranyl Acetate ◽  
Female Rats ◽  
Sprague Dawley ◽  
Rat Mammary Gland ◽  
Intermediate Cells ◽  
Different Cell Types

The mammary gland is composed of epithelial and myoepithelial cells. In the present work, we show that the epithelial component is composed of three types of cells differing in their ultrastructural profiles.Sprague-Dawley virgin female rats, 60 to 100 days old, were sacrificed during estrus. The mammary gland was fixed in Karnovsky's fluid (1), embedded in Epon-Araldite (2), thin-sectioned, stained with uranyl acetate and lead citrate, and examined in an Hitachi HU-11A or a Siemens Elmiskop 1A. To see whether ultrastructural differences correspond to size differences, the nuclear and cytoplasmic areas of 1000 cells were determined from photographs at 10,000X, using a compensating polar planimeter.The population of epithelial cells in the mammary gland is comprised of three different cell types (Fig. 1): a) light cells, b) dark cells, and c) intermediate cells.

scholarly journals Endogenous estrogen mediates vascular reactivity and distensibility in pregnant rat mesenteric arteries

2001 ◽  
Vol 280 (3) ◽  
pp. H956-H961 ◽  
Author(s):  
Yunlong Zhang ◽  
Ken G. Stewart ◽  
Sandra T. Davidge
Keyword(s):  
Vascular Reactivity ◽  
Pressor Response ◽  
Virgin Female ◽  
Mesenteric Arteries ◽  
Female Rats ◽  
Tamoxifen Treatment ◽  
Sprague Dawley ◽  
Arterial Distensibility ◽  
Pregnant Rat ◽  
Endogenous Estrogen

The role of estrogen in the maternal systemic cardiovascular adaptations during pregnancy is still controversial. Female Sprague-Dawley rats were implanted at day 14 of pregnancy with either a 50-mg tamoxifen pellet (estrogen receptor blocker, n = 10) or placebo pellet ( n = 10). Virgin female rats were a nonpregnant control ( n = 7). At days 20–22 of pregnancy, resistance-sized mesenteric arteries were mounted onto a dual-chamber arteriograph system. Pregnancy significantly blunted the pressor response to phenylephrine [measurement of the effective concentration that yielded 50% maximum response (EC50) values were 1.5 ± 0.22 vs. 0.69 ± 0.16 μM ( P < 0.05)] and enhanced vasodilation to ACh [EC50 = 1.13 ± 2.53 vs. 3.13 ± 6.04 nM ( P < 0.05)] compared with nonpregnant rats. However, tamoxifen treatment during pregnancy reversed these effects. Inhibition of nitric oxide (NO) synthase with N G-monomethyl-l-arginine (250 μM) shifted only the responses of the placebo-treated pregnant group to both phenylephrine and ACh. Arterial distensibility in the placebo-treated pregnant group was also significantly increased ( P < 0.05) compared with nonpregnant and tamoxifen-treated pregnant animals. In summary, endogenous estrogen during pregnancy increases NO-dependent modulation of vessel tone and arterial distensibility.

Modeling of fibrocystic mastopathy in experiment on animals

2020 ◽  
Vol 28 (4) ◽  
pp. 429-436
Author(s):  
Svetlana A. Anisimova ◽  
Janna A. Svirina ◽  
Denis A. Maksaev
Keyword(s):  
Mammary Gland ◽  
Virgin Female ◽  
Mammary Glands ◽  
Female Rats ◽  
Fibrocystic Disease ◽  
Drug Induced ◽  
Fibrocystic Mastopathy ◽  
Hormonal Imbalance ◽  
Pathogenetic Factor ◽  
Almost All

Nowadays, hormonal imbalance is proven to be a factor that influences initiation of malignant and benign breast tumors. To study the aspects of participation of sex hormones in damage to organs and tissues, it may be necessary to model a common womens pathology fibrocystic disease of mammary glands characterized by the most pronounced effects of this pathogenetic factor, on experimental animals. Aim. To create a model of fibrocystic disease of mammary gland with the subsequent possibility of studying morphological manifestations of the disease in natural and drug-induced pathomorphism. Materials and Methods. The pathology was induced by intramuscular injection of 0.5 ml of 2% synestrol and 0.5 ml of 2.5% progesterone to virgin female rats on the 1st, 7th, 14th, 21st, 28th and 35th days of the experiment. For examination, histological preparations of inguinal mammary glands were made. The preparations were described and studied using morphometric analysis. Results. In the result of the experiment, pronounced macro- and microscopic alterations of mammary glands were found. Microscopic picture was similar to that observed in fibrocystic mastopathy in women. Almost all the morphometric parameters underwent reliable alterations in correspondence with the given pathology. Conclusion. A model of fibrocystic disease of mammary gland was obtained that may be used for further study of morphogenesis and methods of correction.

scholarly journals Impaired mammary gland T cell population during early lactation in hypoprolactinemic lactation-deficient rats

Reproduction ◽  
2013 ◽  
Vol 146 (3) ◽  
pp. 233-242 ◽  
Author(s):  
Juan Pablo Mackern-Oberti ◽  
Susana Ruth Valdez ◽  
Laura María Vargas-Roig ◽  
Graciela Alma Jahn
Keyword(s):  
Mammary Gland ◽  
T Cell ◽  
Cell Population ◽  
Post Partum ◽  
Lower Percentage ◽  
Corpora Lutea ◽  
Early Lactation ◽  
Sprague Dawley ◽  
Sd Rats ◽  
Antibody Secreting Cells

Mammary stroma is composed of various cell types, including migratory leukocytes. Although mammary antibody-secreting cells have been extensively studied, reports focusing on mammary T cells are scarce. It is thought that the recruitment mechanism of leukocytes to the mammary gland (MG) is controlled by pregnancy- and lactation-specific stimuli. But whether prolactin (PRL) modulates the T-cell population in MG is still unknown. Our aim was to study the relationship between PRL levels and T and B cells during early lactation (L2, day 2 post partum) and mid-lactation (L12, day 12 of lactation). In order to investigate whether PRL is associated with homing events to MG, female Sprague Dawley (SD) and SD-derived desmoglein 4−/− hairless (phenotype with lactation deficit, OFA hr/hr) rats were killed during estrus, pregnancy, and post partum, and blood, MG, and corpora lutea were obtained to perform fluorescent-activated cell sorting (FACS), real-time PCR, and histological and RIA studies. Serum PRL levels were lower in OFA hr/hr rats than in SD rats during early lactation. MG of OFA hr/hr rats showed less secretory material compared with SD rats. FACS analysis showed lower percentage of MG CD3+ cells in OFA hr/hr rats compared with SD rats on L2 and L12. OFA hr/hr rats showed higher absolute numbers of circulating CD3+ cells compared with SD rats on L2 but not on L12. These results show that T-cell population in MG is affected in early lactating OFA hr/hr rats and strongly suggest that serum PRL levels may be involved in the homing events to MG, probably helping antibody-secreting cells and protecting the gland during lactation development.

scholarly journals Tissue-specific ceruloplasmin gene expression in the mammary gland

1991 ◽  
Vol 280 (3) ◽  
pp. 671-677 ◽  
Author(s):  
J L Jaeger ◽  
N Shimizu ◽  
J D Gitlin
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Ductal Carcinoma ◽  
Virgin Female ◽  
Female Rats ◽  
Breast Adenocarcinoma ◽  
Hepatic Tissue ◽  
Tissue Specific ◽  
Mammary Gland Tissue ◽  
Gland Tissue

Using a ceruloplasmin cDNA clone in RNA blot analysis, a single 3.7 kb ceruloplasmin-specific transcript was detected in rat mammary gland tissue from pregnant and lactating animals. Ceruloplasmin gene expression in the mammary gland was tissue-specific, with no evidence of expression in brain, heart or other extrahepatic tissues. Ceruloplasmin mRNA was also detected in mammary gland tissue from male, virgin female and non-pregnant/multiparous animals, and the abundance of ceruloplasmin-specific transcripts in virgin female rats was independent of their stage of oestrus. In virgin female mammary gland the content of ceruloplasmin mRNA was 20% of that in hepatic tissue from these animals and approx. 2-3-fold greater than that found in mammary gland tissue of pregnant or lactating animals. Development studies revealed ceruloplasmin gene expression in male and female mammary gland by only 2 weeks of age, prior to the onset of puberty. Biosynthetic studies indicated that the ceruloplasmin mRNA in mammary gland tissue was translated into a 132 kDa protein qualitatively similar to that synthesized in liver. By in situ hybridization, ceruloplasmin gene expression was localized to the epithelium lining the mammary gland alveolar ducts, without evidence of expression in the surrounding mesenchyme. Ceruloplasmin gene expression was also detected in a human breast adenocarcinoma cell line and in biopsy tissue from women with invasive ductal carcinoma. Taken together, these data indicate that the mammary gland is a prominent site of extrahepatic ceruloplasmin gene expression and add to the evidence that ceruloplasmin biosynthesis is associated with growth and differentiation in non-hepatic tissues.

scholarly journals Immunolocalization of inhibin in the mammary gland of rats treated with hCG.

1993 ◽  
Vol 41 (1) ◽  
pp. 29-34 ◽  
Author(s):  
M V Alvarado ◽  
J Russo ◽  
I H Russo
Keyword(s):  
Mammary Gland ◽  
Polyclonal Antibodies ◽  
Critical Role ◽  
Virgin Female ◽  
Sprague Dawley ◽  
Alveolar Cells ◽  
Glycoprotein Hormone ◽  
Ductal Cells ◽  
Sprague Dawley Rats ◽  
Pre Treatment

Human chorionic gonadotropin (hCG) induces profuse lobular development in the mammary gland of young virgin rats. To clarify whether the effect of hCG is locally mediated by inhibin, a non-steroidal glycoprotein, we detected its localization immunocytochemically in the mammary gland with polyclonal antibodies against the alpha- and beta-chains. Virgin female Sprague-Dawley rats were sacrificed after treatment with a daily IP injection of 100 IU hCG for 5, 10, 15, or 21 days of treatment or 20 days after the last injection. Whereas the mammary gland of control animals did not contain immunoreactive inhibin, hCG treatment induced the expression of inhibin in the cytoplasm of alveolar cells but not in ductal cells. The reaction became evident by Day 10 of treatment and reached its maximal intensity by Day 15. Thereafter, the reaction became evident in the stroma, which exhibited maximal positivity by Day 20. Once hCG treatment was terminated, the mammary gland regressed to its pre-treatment condition, appearing similar both in morphology and inhibin content to that of control animals. The expression of this glycoprotein hormone in the mammary gland after hCG administration at the time of maximal lobulolveolar development, and its diffusion towards the stroma during regression, suggest a critical role of inhibin as a modulator of mammary growth and differentiation.

ULTRASTRUCTURAL CHANGES ACCOMPANYING INVOLUTION OF THE MAMMARY GLAND IN THE ALBINO RAT

1971 ◽  
Vol 51 (1) ◽  
pp. 127-135 ◽  
Author(s):  
R. C. RICHARDS ◽  
G. K. BENSON
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Alveolar Epithelial Cells ◽  
Female Rats ◽  
Ultrastructural Changes ◽  
Albino Rat ◽  
Alveolar Epithelial ◽  
Cellular Debris ◽  
Progressive Necrosis ◽  
Removal Of Fat

SUMMARY Adult female rats undergoing their first lactation were experimentally weaned by removing their pups on day 4 of lactation. The initial phase of mammary gland involution began with the removal of protein granules from the milk by digestion in large stasis vacuoles in the alveolar epithelial cells. Later stages involved a progressive necrosis of the epithelial cells by auto-phagocytosis. Removal of fat droplets and cellular debris occurred at this time and was accomplished by macrophage-like cells. Finally, epithelial cells were detached from the basement membrane and were found, in varying stages of degeneration, lying free in the lumina of the alveoli.

Effects of β-agonist, L-644,969, on adipose depots in growing female rats

1995 ◽  
Vol 75 (1) ◽  
pp. 79-83 ◽  
Author(s):  
J. Zhang ◽  
D. G. Grieve
Keyword(s):  
Mammary Gland ◽  
Dna Content ◽  
Female Rats ◽  
Cell Diameter ◽  
Sprague Dawley ◽  
Fat Percentage ◽  
Fat Cell ◽  
Final Body Weight ◽  
Fat Depots ◽  
Igf I

Growing female Sprague Dawley rats (n = 33) were used to determine the effects of β-agonist, L-644,969, on adipose depots, mammary growth and plasma ST and IGF-I levels. Fat-cell diameter in SF and PF, and mammary DNA content were studied. Rats were allocated to three groups to receive 0,4 or 8 mg kg−1 L-644,969 in powdered diet for 35 d. Compared with control, total mammary gland weight, as a proportion of final body weight, was reduced 14.6 (P < 0.05) and 35.6% (P < 0.01), PF was reduced 30 and 49.6% (both P < 0.01) by 4 and 8 mg kg−1, respectively. The SF was reduced 22.3% (P < 0.05) by β-agonist at 8 mg kg−1 only. In all fat depots, the reductions increased with increasing dose of β-agonist. Carcass fat percentage was reduced by 28.5 and 41.7% (both P < 0.01) in rats fed β-agonist at 4 and 8 ppm, respectively. Fat-cell diameter in both SF and PF was reduced (P < 0.05) (except at 4 ppm level in SF), and mammary DNA content was increased (P < 0.01) in both treatment groups. There was a trend to increased ST concentration but to lower IGF-I concentration as β-agonist levels in diet increased (P > 0.1). The results indicate that β-agonist is effective in reducing body fat deposition and fat-cell size and stimulating mammary gland growth, which may play a role in the control of mammogenesis in growing rats. Key words: Rats, β-agonist, mammary gland, adipose tissue

An adjunct mammary epithelial cell population in parous females: its role in functional adaptation and tissue renewal

Development ◽  
2002 ◽  
Vol 129 (6) ◽  
pp. 1377-1386 ◽  
Author(s):  
Kay-Uwe Wagner ◽  
Corinne A. Boulanger ◽  
MaLinda D. Henry ◽  
Magdalene Sgagias ◽  
Lothar Hennighausen ◽  
...  
Keyword(s):  
Cell Death ◽  
Mammary Gland ◽  
Epithelial Cell ◽  
Cell Population ◽  
Mammary Epithelial Cell ◽  
Mammary Epithelial ◽  
Functional Adaptation ◽  
Alveolar Cells ◽  
Genetically Engineered Mice ◽  
Epithelial Cell Population

Mammary gland biologists have long assumed that differentiated secretory epithelial cells undergo programmed cell death at the end of lactation and that the alveolar compartment is reconstituted from undifferentiated precursor cells in subsequent pregnancies. It is generally agreed that the remodeled gland in a parous animal resembles that of a mature virgin at the morphological level. However, several physiological differences have been noted in comparing the responses of mammary epithelia from nulliparous versus parous females to hormonal stimulation and carcinogenic agents. We present genetic evidence that an involuted mammary gland is fundamentally different from a virgin gland, despite its close morphological resemblance. This difference results from the formation of a new mammary epithelial cell population that originates from differentiating cells during pregnancy. In contrast to the majority of fully committed alveolar cells, this epithelial population does not undergo cell death during involution or remodeling after lactation. We show that these cells can function as alveolar progenitors in subsequent pregnancies and that they can play an important role in functional adaptation in genetically engineered mice, which exhibit a reversion of a lactation-deficient phenotype in multiparous animals. In transplantation studies, this parity-induced epithelial population shows the capacity for self-renewal and contributes significantly to the reconstitution of the resulting mammary outgrowth (i.e. ductal morphogenesis and lobulogenesis). We propose that this parity-induced population contributes importantly to the biological differences between the mammary glands of parous and nulliparous females.

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