Growth and differentation of rat mammary epithelial cells cultured in serum-free medium

1997 ◽  
Vol 20 (4) ◽  
pp. 297-305 ◽  
Author(s):  
Dong Yeum Kim ◽  
Byung-Hak Jhun ◽  
Kyung Hee Lee ◽  
Seung Chul Hong ◽  
Kelly H. Clifton ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
Cells Cultured

All-trans retinoic acid induced differentiation of rat mammary epithelial cells cultured in serum-free medium

1998 ◽  
Vol 21 (3) ◽  
pp. 298-304 ◽  
Author(s):  
Min Hyo Ki ◽  
Kee-Joo Paik ◽  
Ji Hyeon Lee ◽  
Hae Young Chung ◽  
Kyung Hee Lee ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
Trans Retinoic Acid ◽  
All Trans Retinoic Acid ◽  
Cells Cultured

scholarly journals Protection of bovine mammary epithelial cells from hydrogen peroxide-induced oxidative cell damage by selenium

2018 ◽  
Vol 63 (No. 3) ◽  
pp. 94-102
Author(s):  
Y.M. Guo ◽  
J. Gong ◽  
Y.G. Zheng ◽  
B.L. Shi ◽  
X.Y. Guo ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Epithelial Cells ◽  
Oxidative Damage ◽  
Mammary Epithelial Cells ◽  
Mapk Pathway ◽  
Mammary Epithelial ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
Bovine Mammary Epithelial Cells

The uncontrolled release of arachidonic acid (ARA) and its metabolism by lipoxygenase (LOX) pathway can induce and aggravate cellular oxidative stress. Selenium (Se) is an integral part of some antioxidative selenoproteins and may protect cells from oxidative damage by modulating ARA release and metabolism. The present study aimed to investigate the protective response of Se against hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>)-induced oxidative damage in bovine mammary epithelial cells (BMECs). The BMECs were incubated for 24 h in serum-free medium and then divided into four groups randomly. The cells in groups 1 and 2 were subsequently incubated for 30 h in serum-free medium containing 0 (control) and 50 nM Se (Se treatment group). The cells in groups 3 and 4 were incubated for 24 h in serum-free medium containing 0 and 50 nM Se, and then treated with 600 μM H<sub>2</sub>O<sub>2</sub> for 6 h (H<sub>2</sub>O<sub>2</sub> damage group and Se prevention group). The results showed that Se attenuated the H<sub>2</sub>O<sub>2</sub>-induced production of reactive oxygen species and the decrease of antioxidative enzymes as glutathione peroxidase (GPX), thioredoxin reductase (TrxR), selenoprotein P (SelP), superoxide dismutase, and catalase in BMECs. The preventive effects of Se on the decrease of selenoprotein activity were demonstrated further by the increase of mRNA expression for GPX1, TrxR1, and SelP, and protein expression for GPX1 and TrxR1. Pretreatment of cells with Se inhibited the H<sub>2</sub>O<sub>2</sub>-induced increase of mRNA expressions and activities for cytosolic phospholipase A2 and 5-lipoxygenase, ARA release, and 15-hydroperoxyeicosatetraenoic acid production. Se also blocked the H<sub>2</sub>O<sub>2</sub>-induced activation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase but not that of extracellular signal-regulated kinase. These results suggested that Se may protect BMECs against H<sub>2</sub>O<sub>2</sub>-induced oxidative damage by increasing selenoproteins synthesis, inhibiting MAPK pathway, and then decreasing ARA release and its metabolism by LOX pathway.

Metabolism of 7,12-dimethylbenz[a]anthracene by mouse mammary epithelial cells cultured serum-free inside collagen gels

1988 ◽  
Vol 40 (2) ◽  
pp. 123-132 ◽  
Author(s):  
Raphael C. Guzman ◽  
Rebecca C. Osborn ◽  
Jack C. Bartley ◽  
Satyabrata Nandi
Keyword(s):  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Collagen Gels ◽  
Serum Free ◽  
Cells Cultured

Lactoferrin expression in mammary epithelial cells is mediated by changes in cell shape and actin cytoskeleton

1997 ◽  
Vol 110 (22) ◽  
pp. 2861-2871 ◽  
Author(s):  
M.J. Close ◽  
A.R. Howlett ◽  
C.D. Roskelley ◽  
P.Y. Desprez ◽  
N. Bailey ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Mammary Gland ◽  
Cell Shape ◽  
Mammary Epithelial Cells ◽  
Mammary Epithelial ◽  
Serum Free Medium ◽  
Free Medium ◽  
Serum Free ◽  
Physical Constraints ◽  
Beta Casein

Lactoferrin is a secreted iron binding protein which is expressed during normal functional development of mammary epithelium. Murine mammary epithelial cell lines competent for milk protein expression were used to identify microenvironmental factors that regulate lactoferrin expression. While lactoferrin was not expressed in adherent monolayer cultures under standard subconfluent conditions on plastic, lactoferrin mRNA and protein steadily accumulated when the cells aggregated to form spheroids on a reconstituted basement membrane gel. However, unlike other milk proteins such as beta-casein, lactoferrin expression was also induced at high cell density in the absence of exogenously added basement membrane or prolactin. These results led us to examine whether changes in cell growth, cell-cell interactions and/or cell shape were responsible for regulation of lactoferrin gene expression. Rounded, non-proliferating cells in suspension in serum-free medium expressed lactoferrin even as single cells. Conversely, lactoferrin expression could be inhibited in non-proliferative cells in serum-free medium by maintaining them in contact with an air-dried extracellular matrix which caused the cells to retain flat, spread morphologies. These findings indicated that cessation of cell growth was not sufficient, that cell-cell interactions were not required, and that cell culture conditions which minimize cell spreading may be important in maintaining lactoferrin expression. Additional data supporting this latter concept were generated by treating spread cells with cytochalasin D. The resulting disruption of microfilament assembly induced both cell rounding and lactoferrin expression. Shape-dependent regulation of lactoferrin mRNA was both transcriptional and post-transcriptional. Surprisingly, treatment of rounded cells with a transcription inhibitor, actinomycin D, produced a stabilization of lactoferrin mRNA, suggesting that transcription of an unstable factor is required for degradation of lactoferrin mRNA. Importantly, lactoferrin mRNA expression was regulated similarly in early passage normal human mammary epithelial cells. In vivo, the changing extracellular matrix components of the mammary gland during different stages of normal and abnormal growth and differentiation may provide different physical constraints on the configurations of cell surface molecules. These physical constraints may be communicated to the cell interior through mechanical changes in the cytoskeleton. Unlike beta-casein whose expression is upregulated by specific integrin-mediated signals, lactoferrin may be representative of a class of proteins synthesized in the mammary gland using basal transcriptional and translational machinery. The suppression of lactoferrin expression that is observed in monolayer culture and in malignant tissues may reflect inappropriate cell shapes and cytoskeletal structures that are manifested under these conditions.

Human endometrial epithelial cells grown on collagen in serum-free medium. Estrogen responsiveness and morphology

1991 ◽  
Vol 125 (1) ◽  
pp. 101-108 ◽  
Author(s):  
Bertil G. Casslén ◽  
Michael J. K. Harper
Keyword(s):  
Epithelial Cells ◽  
Primary Cultures ◽  
Collagen Matrix ◽  
Human Endometrium ◽  
Serum Free Medium ◽  
Free Medium ◽  
Endometrial Stromal Cells ◽  
Prolonged Incubation ◽  
Serum Free ◽  
Endometrial Epithelial Cells

Abstract. The aim of the study was to explore the possibility of using human endometrial epithelial cells in serum-free culture as a sensitive assay for hormonal effects on the human endometrium. Glands were isolated following enzymatic digestion of the endometrial tissue and plated on a collagen matrix. The epithelial cells were grown in either medium containing serum or in supplemented serum-free medium. No morphologic difference was found between cells grown in these two media for up to 5 days, using either light or scanning electron microscopy. Secretion of prostaglandin F2α (PGF2α) in response to estradiol was not lower in serum-free medium than in medium containing serum for the first 2 days of culture, whereas secretion declined after prolonged incubation in the serum-free medium. This response to estradiol was clearly dose-dependent, and it was further enhanced by addition of arachidonic acid, the precursor for prostaglandin synthesis, to the medium. Co-culture of endometrial stromal cells did not influence the secretion of PGF2α by epithelial cells. We conclude that the secretion of PGF2α from primary cultures of human endometrial epithelial cells grown on collagen in serum-free medium can be used for a limited period as an assay of estrogenic effects on the human endometrium.

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