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At least 19 recordsLinked to original sources
PubMed2001

Escherichia coli induces apoptosis and proliferation of mammary cells.

Mammary cell apoptosis and proliferation were assessed after injection of Escherichia coli into the left mammary quarters of six cows. Bacteriological analysis of foremilk samples revealed coliform infection in the injected quarters of four cows. Milk somatic cell counts increased in these quarters and peaked at 24 h after bacterial injection. Body temperature also increased, peaking at 12 h postinjection. The number of apoptotic cells was significantly higher in the mastitic tissue than in the uninfected control. Expression of Bax and interleukin-1beta converting enzyme increased in the mastitic tissue at 24 h and 72 h postinfection, whereas Bcl-2 expression decreased at 24 h but did not differ significantly from the control at 72 h postinfection. Induction of matrix metalloproteinase-9, stromelysin-1 and urokinase-type plasminogen activator was also observed in the mastitic tissue. Moreover, cell proliferation increased in the infected tissue. These results demonstrate that Escherichia coli-induced mastitis promotes apoptosis and cell proliferation.

Animals↗
PubMed1994

Characterization of plasma and intracellular membrane prolactin receptor in lactating mouse mammary cells.

Mammary cells were prepared from lactating mice by collagenase digestion in order to examine the reaction of prolactin (PRL) with its cellular receptors. Cells were treated with 10% acetic acid following PRL binding. Between 5 and 12.5% acetic acid, the dissociation of PRL remained constant. The ratio of dissociated PRL was comparable to that of tissue slices or disrupted cells with this treatment. In subcellular membranes, about 81% of PRL bound to plasma membrane receptors was dissociated by acid treatment while PRL dissociated from intracellular membrane receptors was about 21%. Based on the nature of their PRL dissociation, PRL receptors were classified as acid-sensitive or acid-insensitive. The reaction of PRL with either species was reversible and saturable, and was dependent on temperature and time. Both species showed high PRL-binding affinity. However, acid-insensitive receptor was unstable at 37 degrees C. The level of acid-sensitive receptor was close to that of acid-insensitive receptor in late pregnancy. During the first 3 days of lactation, the level of acid-sensitive receptor increased more slowly than that corresponding to acid-insensitive receptor. The above criteria suggest that the postpartum increase in PRL binding is characterized especially by an increase in the level of acid-insensitive PRL receptor located mainly on intracellular membrane.

Acetates↗
PubMed2000

Nutritional and somatotropin regulation of the mitogenic response of mammary cells to mammary tissue extracts.

Our objective was to investigate the mitogenic response of primary mammary epithelial cells to extracts of mammary parenchyma from 24 prepubertal Friesian heifers treated with placebo or growth hormone at either a low or a high feeding level. The mitogenic responses to mammary extracts were tested by using primary mammary epithelial organoids obtained from prepubertal heifers cultured for 4 to 5 d in collagen gels in serum-free medium supplemented to 5% concentration of the mammary extracts. Cell proliferation was determined using [methyl-3H]thymidine incorporation as a measure of DNA synthesis. High feeding level reduced DNA synthesis in response to mammary extracts. At low feeding level, growth hormone treatment decreased DNA synthesis in response to mammary extracts whereas, at high feeding level, growth hormone increased DNA synthesis in response to mammary extracts. These results suggest that locally produced growth factors are involved in the regulation of mammary development when mammary growth is modulated by feeding level and growth hormone treatment.

Animal Feed↗
PubMed2005

Stromal regulation of neoplastic development: age-dependent normalization of neoplastic mammary cells by mammary stroma.

There is mounting evidence that the stroma plays a crucial role in mammary gland carcinogenesis. Here, we report that mammary gland stroma from mature and multiparous rats prevents neoplastic development and encourages normal ductal growth of grafted epithelial cancer cells. Fifty thousand epithelial cancer cells were injected into the cleared fat pads of virgin hosts at 24, 52, 80, and 150 days of age and of hosts that had undergone two cycles of pregnancy, lactation, and involution. Six months after inoculation, tumor incidence was 75%, 100%, 50%, and 18.2% in 24-, 52-, 80-, and 150-day-old virgin rats, respectively, and 0% in the twice-parous animals. Most remarkably, these neoplastic cells appeared to form normal ducts in all hosts-Ha-ras-1 mutation served as a marker to identify the tumor origin of the outgrowths. The tumor development pattern suggests a parallel to the phenomenon of age- and reproductive state-dependent susceptibility and resistance to chemical carcinogens. As susceptibility to carcinogenesis decreases, the ability of the stroma to reprogram neoplastic epithelial cells increases. Thus, the neoplastic phenotype is context-dependent, and it therefore offers the intriguing possibility that the process of carcinogenesis is amenable to normalization or cure once the mechanisms of stroma-mediated normalization are elucidated and manipulated.

Aging↗
PubMed1998

[EGF-dependent epithelial cells of the mammary cell line HC11 demonstrate a high degree of synchronized cell cycle during stimulation with epidermal growth factor].

The most popular object for studying endocytosis of EGF-receptor complexes, human epidermoid carcinoma A431, was shown to answer to EGF in high concentration (100 ng/ml) by growth inhibition, being indifferent to lower (0.1-1 ng/ml) concentrations. At the same time, cells NIH 3T3, expressing human EGF receptor (HER14), and epithelial mammary cells HC11 increased 14C-thymidine incorporation into DNA after EGF addition. However, for HER14 cells stimulatory effect of EGF was twice weaker than that induced by serum, whereas the effect of EGF on 14C-thymidine incorporation in DNA of cells HC11 was approximately 5 times stronger compared to serum. Therefore, cells HC11 may be referred to as EGF-dependent. Cell cycle analysis by fluorimetry showed that more than 90% of serum-starved HER14 and HC11 were in G0/G1. Within 19-20 h after stimulation by EGF 70-90% of HC11 cells and only 30-40% of HER14 cells were in S-phase. EGF removing from culture medium earlier than 9-11 h after stimulation blocked entering of HC11 cells into S-phase, whereas such EGF-dependent period was not found for cells HER14. Thus, synchronization of progression through early stages of cell cycle, stimulated by EGF and the presence of well defined "early" (EGF-dependent) and "late" (EGF-independent) phases, make cells HC11 convenient object for studying physiological role of EGF receptor complexes endocytosis.

Animals↗
PubMed1981

Fibronectin production by human mammary cells.

Human mammary cells were examined for the presence of the high-molecular-weight surface glycoprotein fibronectin. Early passage mammary epithelial cell and fibroblast cultures from both carcinomas and normal tissues were tested for the presence of cell-associated fibronectin by immunofluorescence microscopy and for the synthesis and secretion of fibronectin by specific immunoprecipitation of metabolically labeled protein. In vivo frozen sections of primary carcinomas and normal tissues were tested for the localization of fibronectin by immunofluorescence microscopy. In contrast to the extensive fibrillar networks of fibronectin found in the fibroblast cultures, the epithelial cell cultures from both tissue sources displayed a pattern of cell-associated fibronectin characterized by powdery, punctate staining. However, the cultured epithelial cells, as well as the fibroblasts, secreted large quantities of fibronectin into the medium. Putative myoepithelial cells also displayed extensive fibrillar networks of fibronectin. The difference in cell-associated fibronectin distribution between the epithelial cells and the fibroblasts and putative myoepithelial cells provided a simple means of quantitating stromal and myoepithelial cell contamination of the mammary epithelial cells in culture. In vivo, normal tissues showed fibronectin primarily localized in the basement membrane surrounding the epithelial cells and in the stroma. Most primary carcinomas displayed powdery, punctate staining on the epithelial cells in addition to the fibronectin present in the surrounding stroma.

Basement Membrane↗
PubMed1985

Estrogen responsiveness of normal mouse mammary cells in primary cell culture: association of mammary fibroblasts with estrogenic regulation of progesterone receptors.

Estrogens enhance proliferation of normal mouse mammary cells in vivo. However, when cultured alone, normal mouse mammary epithelial cells fail to exhibit a proliferative response to estrogen in vitro; the basis for this lack of in vitro responsiveness to estrogen is not known. The purpose of the present study is to determine if cultured normal mouse mammary cells possess estrogen receptors (ER) and/or progesterone receptors (PgR) and if the ER mechanism is functional, as measured by the ability of estrogens to regulate PgR. Recent findings that mammary fibroblasts can influence the behavior of mammary epithelial cells in vitro led us to investigate their effect on epithelial cell responsiveness to estrogen. In these studies, collagenase-dissociated mammary glands of midpregnant BALB/c mice were the source of mixed cultures (containing both epithelial cells and fibroblasts) and epithelial or fibroblast cultures. The purity of epithelial or fibroblast cultures was quantified immunocytochemically using antivimentin antibody as a fibroblast marker. Steroid hormone binding was quantified in intact cultured cells using [3H]R5020 and 17 beta-[3H]estradiol as the ligands. Specific high affinity binding sites for estrogen (Kd = 3.1 +/- 0.8 X 10(-10] and progestins (Kd = 3.3 +/- 1.2 X 10(-9) M) were detected in mixed cultures. To assess the possible role of mammary fibroblasts, we investigated cultures containing only fibroblasts which were derived by differential centrifugation. When 17 beta-estradiol was added to the culture medium, a significant (P less than 0.01) increase in PgR concentration was observed in mixed cultures. While mixed cultures maintain responsiveness to estrogen in vitro, as measured herein, the epithelial cultures, derived by differential centrifugation and Percoll gradient sedimentation, did not. However, estrogenic regulation of PgR appears to be specific to epithelial cells in mixed cultures, since fibroblast cultures neither contained PgR nor displayed estrogen-inducible PgR. The lack of responsiveness of epithelial cultures is not due to a loss or decrease in the ER concentration. Thus, the presence of mammary fibroblasts appears to be associated with epithelial cell responsiveness to estrogen in vitro.

Animals↗
PubMed1987

Interspecies differences in the major DNA adducts formed from benzo(a)pyrene but not 7,12-dimethylbenz(a)anthracene in rat and human mammary cell cultures.

Mammary epithelial cells from rats and humans show both quantitative and qualitative species- and carcinogen-specific differences in their abilities to activate benzo(a)pyrene (B(a)P) and 7,12-dimethylbenz(a)anthracene (DMBA). Previous studies of the DNA binding of these compounds in mammary epithelial cells demonstrated that rat cells bound relatively more DMBA than B(a)P to DNA under identical treatment conditions, while the opposite pattern was exhibited by human mammary epithelial cells. The specific DNA adducts formed in these cells after 24-h incubations with [3H]DMBA and [3H]B(a)P were analyzed to determine if there were qualitative as well as quantitative differences in the amounts of individual adducts. Similar proportions of specific DMBA-DNA adducts were found in both rat and human cells, although the total amount of adducts formed was significantly higher in the rat cells. In contrast, an essentially qualitative species-specific difference was observed in the major B(a)P-DNA adduct present in the rat and human cells. The major B(a)P adduct formed in the human mammary epithelial cells was identified as the (+)-anti-B(a)P-7,8-dihydrodiol-9, 10-epoxide(BPDE)-deoxyguanosine adduct. However, this adduct was formed at very low levels in the rat mammary epithelial cells. The rat cells contained a large proportion of syn-BPDE adducts, and other unidentified B(a)P-DNA adducts. The high level of the (+)-anti-BPDE-deoxyguanosine adduct in the human but not the rat mammary cells is consistent with the potential role of (+)-anti-BPDE in the high mutagenic activity of B(a)P in the cell-mediated mutagenesis assays using the human mammary cells as activators, and the low mutagenic activity of B(a)P when rat cells were used as activators. The quantitative differences in the activation of DMBA by cells from these two species are also consistent with the cell-mediated mutagenic activities of DMBA using these cells as activators. These results suggest that the higher carcinogenic activity of DMBA compared to B(a)P in the rat mammary gland may not be indicative of the relative carcinogenic potencies of these compounds for human mammary cells.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed1988

Insufficiency of transformation by simian virus 40, polyomavirus, EJ-ras, or v-myc oncogenes for conversion of ethanolamine-responsive mammary cells to ethanolamine-nonresponsive cells.

Normal mammary epithelial cells (ethanolamine responsive) require ethanolamine to enable them to grow in defined culture medium because they cannot synthesize de novo a sufficient amount of phosphatidylethanolamine. Mammary tumor cells which retain properties of the normal tissue are also likely to be ethanolamine responsive, whereas dedifferentiated, highly tumorigenic mammary tumor cells are ethanolamine nonresponsive. The nonresponsive tumor cells are able to synthesize the necessary amount of phosphatidylethanolamine to sustain growth. Therefore, the progression of malignancy seems to convert ethanolamine-responsive mammary cells to ethanolamine-nonresponsive ones. In an attempt to prove the above assumption and to understand the mechanism responsible for the conversion during the progression of malignant transformation, mammary tumor cell line 64-24, which is typically ethanolamine responsive, was transfected with simian virus 40, polyomavirus, EJ-ras, or v-myc oncogenes, and the resulting transfectants were examined for their growth response to ethanolamine. Many of the transfectants exhibited typical transformed phenotypes; however, none of the transfectants converted to ethanolamine-nonresponsive cells. Some of the SV40 and polyomavirus transformants were able to grow in the absence of ethanolamine, although they grew better in the presence of ethanolamine, unlike typical ethanolamine-nonresponsive cells. These cells could grow in the absence of ethanolamine, even though their membrane phospholipid was phosphatidylethanolamine deficient. The present study indicates that the expression of any one of the four oncogenes tested, which allows the cells to exhibit transformed phenotypes in 64-24 cells, is not sufficient for the conversion of ethanolamine-responsive cells to -nonresponsive cells.

Animals↗
PubMed2006

Cyclooxygenase-2 expression in normal and neoplastic canine mammary cell lines.

Mammary cancer is the most common cancer in female dogs. Induction of cyclooxygenase-2 (COX-2), a key enzyme in prostaglandins (PGs) biosynthesis, has been demonstrated in various cancers in humans and dogs, including mammary cancer. The objective of this study was to investigate the expression and regulation of COX-2 in canine mammary epithelial cells. Cell lines derived from normal and neoplastic canine mammary glands were cultured in the absence or presence of phorbol 12-myristate 13-acetate (PMA), and immunoblots, immunocytochemistry, radioimmunoassays, and a cell proliferation assay were used to study COX-2 expression and PGs production. Results showed that the neoplastic cell line CMT12 constitutively overexpressed COX-2 protein whereas other mammary cell lines expressed low to undetectable basal levels of COX-2 protein. Basal PGE(2) production was significantly higher (P < .05) in CMT12 compared to other cell lines. Levels of COX-2 protein in CMT12 decreased in a time-dependent manner with serum starvation, and PMA stimulation induced a strong time-dependent increase in COX-2 protein. Treatment of CMT12 cells with NS-398 (a specific COX-2 inhibitor) significantly blocked PGE(2) synthesis and reduced cell proliferation (P < .05). These results indicate that some neoplastic canine mammary cell lines constitutively overexpress COX-2, and that COX-2 inhibition decreases PGE(2) production and cell proliferation, supporting a role for COX-2 and PGs in canine mammary oncogenesis.

Animals↗
PubMed2002

Proteomic patterns of cultured breast cancer cells and epithelial mammary cells.

Breast cancer is one of the leading causes of death from cancer among women in western countries. The different types of breast cancer are grouped into invasive and noninvasive forms. Among the invasive types, ductal infiltrating carcinoma (DIC) is the most common and aggressive form. Using an in vitro model consisting of a DIC-derived cell line (8701-BC) and a nontumoral mammary epithelial cell line (HB2), we used the proteomics approach to search for homology and differences in protein expression patterns between tumoral and nontumoral phenotypes. Within an analysis window comprising 1,750 discernible spots we have currently catalogued 140 protein spots of potential interest. Fifty-eight of them were identified by gel matching with reference maps, immunodetection, or N-terminal microsequencing and classified into four functional groups. Twelve proteins were found differentially expressed in two cell lines: four were uniquely present in the neoplastic cell proteome and eight in epithelial cells. In addition, 53 proteins displayed different relative expression levels between the two cell lines, that is, 44 were more elevated in cancer cells and 9 in HB2 cells. Among proteins with greater relative abundance in cancer cells we identified glycolytic enzymes (or their isoforms), which may indicate that the known metabolic dysregulation in cancer can reflect oncogenic-related defects of glycolytic gene expression.

Breast↗
PubMed1985

Specific neutralizing antiserum against a polypeptide growth inhibitor for mammary cells purified from bovine mammary gland.

A recently published method for purification of a new inhibitor of growth of mammary cells in vitro from bovine mammary gland has been modified to yield several hundred micrograms of inhibitor per kg of glandular tissue. The inhibitory effect exerted by this preparation to Ehrlich ascites mammary carcinoma cells fulfilled all biological criteria of specificity established earlier for preparations obtained by other means, the most important being that the inhibitory effect is abolished by the epidermal growth factor and insulin. The preparation is shown to consist mainly of a protein of 13 kDa which appears to be not glycosylated. An antiserum raised in mice against the inhibitor is demonstrated to be specific for the 13 kDa bovine mammary gland protein. Neutralization of the inhibitory activity by the specific antiserum strongly supports the view that the 13 kDa protein is indeed the carrier of inhibitory activity. First data on tissue distribution obtained with an enzyme-linked immunosorbent assay revealed a high concentration of the anti-inhibitor-antiserum-reactive antigen in bovine lactating but not in non-lactating mammary gland tissue and in milk fat globule membranes. Some reactivity was also found in bovine lung. These data are interpreted with respect to a possible physiological significance of the growth inhibitor.

Animals↗
PubMedDate not supplied

A bcl-xS adenovirus selectively induces apoptosis in transformed cells compared to normal mammary cells.

Oncogenes which drive the cell cycle, such as c-myc, can sensitize cells to apoptosis. This suggests the possibility that the expression of genes such as bcl-2 or bcl-xL is required to inhibit apoptosis induced by oncogene expression. We hypothesized that inhibition of Bcl-2/Bcl-xL by the pro-apoptotic Bcl-xS protein, would result in selective induction of apoptosis in mammary carcinoma cells compared to their nontransformed counterparts. Therefore, we compared the effects of Bcl-xS expression delivered by a bcl-xS adenovirus (bcl-xS-Adv) vector, on viability and apoptosis of nontransformed versus transformed mammary epithelial cells. We report that c-myc-transformed murine mammary cells are extremely sensitive to apoptosis induced by the bcl-xS adenovirus (bcl-xS-Adv) vector, whereas immortalized, nontransformed murine mammary cells are relatively resistant to apoptosis induced by this vector. Likewise, human mammary epithelial cells transduced with c-erbB-2 were more sensitive to apoptosis induced by the bcl-xS vector than the nontransformed parental cells. Similar results were obtained when we tested the effects of bcl-xS adenoviral infection on primary normal human mammary epithelial cells and SUM-190 PT cells, (a c-erbB-2 over-expressing human mammary carcinoma cell line) grown on Matrigel. These data are consistent with the hypothesis that inhibition of Bcl-2/Bcl-xL can result in selective killing of cancer cells compared to their nontransformed counterparts.

Adenoviridae↗
PubMed1981

Generation of fibroblast-like cells from cloned epithelial mammary cells in vitro: a possible new cell type.

We have isolated clonal cell lines from a nitrosomethylurea-induced mammary tumor in Wistar--Furth rats. The epithelial-like cells of these lines give rise to fibroblast-like cells. A study of several markers showed that the epithelial-like cells are similar to epithelial mammary cells. The fibroblastic cells, however, were similar to stromal cells, except for the production of collagen IV. The events occurring in these cultures are identical to those observed in previously isolated mammary cultures [Bennett, D. C., Peachey, L. A., Durbin, H. & Rudland, P. S. (1976) Cell 15, 283--298], suggesting their generality. The fibroblast-like cells generated in culture may be a hitherto unrecognized type of mammary cell.

Animals↗
PubMed1988

Substratum modulation of epidermal growth factor receptor expression by normal mouse mammary cells.

Normal mouse mammary cells synthesize the basement membrane scaffold on which the cells rest in vivo. This extracellular matrix material serves important functions in the growth and differentiation of the mammary epithelium. Components of the basement membrane negatively regulate basement membrane collagen biosynthesis in response to epidermal growth factor stimulation. This effect is shown to correlate with changes in growth factor receptor regeneration following ligand-induced receptor down-regulation. The results suggest that while control of basement membrane synthesis may be manifest in part by the availability of growth factors, the environment in which the mammary cell finds itself is also very important.

Animals↗
PubMed1999

Cell cycle analysis of cultured porcine mammary cells.

One of the major points of debate in determining the effectiveness of nuclear transfer technology has been the phase of the cell cycle of the donor cell at the time of nuclear transfer. Here, a primary mammary cell line has been isolated and various treatments for synchronization of the cell cycle have been tested. The cells were then simultaneously stained for DNA content and protein content and the percentages of cells in G1, G0, S, and G2 + M were estimated. In the first experiment, cells were either cycling, grown to confluence, or serum-starved for 5 days. Serum starvation increased (p < 0.05) the percentage of cells in G0 compared to confluent or cycling cells from 3% to 8% to 22%. By using forward scatter to determine the size of the cells it was determined that if small cells (7-15 microm) were selected from the serum-starved group 43.9% will be in G(0) as compared to 4.5% of cycling cells and 9.9% of confluent cells. Dimethyl sulfoxide (DMSO) treatment (0%, 0.5%, or 1.0%) for 72 hours (shown to synchronize some cell types in G0) had no effect on the percentage of cells in G0, G1, S, or G2 + M. Treatment with mimosine (0 microM, 0.4 microM, 0.8 microM or 1.2 microM), a compound that should synchronize the cells in G1, increased (p < 0.05) the percentage of cells in G1 from 66.7% (0 microM mimosine) to 79.0% to 82.0%. Finally, treatment with colchicine for 24 hours (shown to synchronize some cell types in G2 + M) increased (p < 0.05) the percentage of cells in G2 + M (0 microM colchicine) from 13.3% to 27.2% to 31.6%. It is concluded that many cell cycle synchronization techniques are effective in porcine mammary cell lines, but none of the techniques are 100% effective. Such results should help elucidate the mechanisms involved in nuclear transfer.

Animals↗
PubMed1989

Production of mammastatin, a tissue-specific growth inhibitor, by normal human mammary cells.

The growth of human mammary cells may be regulated by a balance between growth stimulatory and growth inhibitory pathways. Polypeptides of 47 and 65 kilodaltons (mammastatin) were isolated from conditioned medium of normal human mammary cells. Monoclonal antibodies against mammastatin were generated that blocked its activity and were used for purification and further characterization of the protein. Mammastatin inhibited the growth of 5 transformed human mammary cell lines, but had no effect on the growth of 11 transformed human cell lines derived from nonmammary tissues. Mammastatin appeared to be a heat-labile protein distinct from transforming growth factor-beta (TGF-beta). By immunoperoxidase staining it was detected in cultured normal human mammary cells, but was decreased in transformed mammary cells.

Antibodies, Monoclonal↗
PubMed1998

Effect of substratum on growth, cell morphology and lactoferrin synthesis and secretion in bovine mammary cell culture.

The role of extracellular matrix in morphology, growth and lactoferrin synthesis and secretion in bovine mammary cells from a developing gland is poorly defined. In this study, bovine mammary cells from a hormone-primed developing gland were isolated and cultured on plastic, collagen, embedded within collagen, or on EHS-matrix, with the hormones prolactin, insulin, and cortisol in the presence or absence of fetal calf serum. Mammary cells on plastic or collagen spread and formed confluent cells sheets, while those embedded within collagen or on EHS-matrix maintained their acinar-like structure. Histological and ultrastructural analysis of cells showed that cells on plastic and collagen grew in multilayers, while those embedded within collagen or on EHS-matrix lacked any lumen structure. The ultrastructure of cells on different substrata more resembled an undifferentiated phenotype. Mammary cells secreted lactoferrin in increasing concentrations throughout the culture period. The total amount secreted in culture was regulated by extracellular matrix and fetal calf serum. Cells embedded within collagen in serum-free cultures secreted the lowest amounts of lactoferrin (up to 619 ng/ml; day 14), while those on collagen and supplemented with fetal calf serum secreted up to 4920 ng/ml at day 14. Fetal calf serum induced higher lactoferrin secretion within each substratum on which the cells were cultured. No intracellular accumulation of lactoferrin was noted in cells on plastic or collagen or those embedded within collagen, whereas those on EHS-matrix accumulated more than 500 ng/ml of lactoferrin intracellularly/intracinarly. Furthermore, when cultured on a similar substratum, cells from a developing gland secreted higher lactoferrin than cells from a lactating gland.

Animals↗