Analysis of the Involuting Mouse Mammary Gland: An In Vivo Model for Cell Death

2016 ◽  
pp. 165-186 ◽  
Author(s):  
Bethan Lloyd-Lewis ◽  
Timothy J. Sargeant ◽  
Peter A. Kreuzaler ◽  
Henrike K. Resemann ◽  
Sara Pensa ◽  
...  
Keyword(s):  
Cell Death ◽  
Mammary Gland ◽  
Mouse Mammary Gland ◽  
In Vivo Model

scholarly journals Tumor cytotoxicity and immunogenicity of a novel V-jet neon plasma source compared to the kINPen

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Lea Miebach ◽  
Eric Freund ◽  
Stefan Horn ◽  
Felix Niessner ◽  
Sanjeev Kumar Sagwal ◽  
...  
Keyword(s):  
Cell Death ◽  
Dendritic Cells ◽  
Cancer Cells ◽  
Treatment Time ◽  
Plasma Source ◽  
In Vivo Model ◽  
Antitumor Effects ◽  
Plasma Device

AbstractRecent research indicated the potential of cold physical plasma in cancer therapy. The plethora of plasma-derived reactive oxygen and nitrogen species (ROS/RNS) mediate diverse antitumor effects after eliciting oxidative stress in cancer cells. We aimed at exploiting this principle using a newly designed dual-jet neon plasma source (Vjet) to treat colorectal cancer cells. A treatment time-dependent ROS/RNS generation induced oxidation, growth retardation, and cell death within 3D tumor spheroids were found. In TUM-CAM, a semi in vivo model, the Vjet markedly reduced vascularized tumors' growth, but an increase of tumor cell immunogenicity or uptake by dendritic cells was not observed. By comparison, the argon-driven single jet kINPen, known to mediate anticancer effects in vitro, in vivo, and in patients, generated less ROS/RNS and terminal cell death in spheroids. In the TUM-CAM model, however, the kINPen was equivalently effective and induced a stronger expression of immunogenic cancer cell death (ICD) markers, leading to increased phagocytosis of kINPen but not Vjet plasma-treated tumor cells by dendritic cells. Moreover, the Vjet was characterized according to the requirements of the DIN-SPEC 91315. Our results highlight the plasma device-specific action on cancer cells for evaluating optimal discharges for plasma cancer treatment.

scholarly journals In vivo MRI of early stage mammary cancers and the normal mouse mammary gland

2011 ◽  
Vol 24 (7) ◽  
pp. 880-887 ◽  
Author(s):  
Sanaz A. Jansen ◽  
Suzanne D. Conzen ◽  
Xiaobing Fan ◽  
Erica Markiewicz ◽  
Thomas Krausz ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Normal Mouse ◽  
Early Stage ◽  
Mouse Mammary Gland

RAPIDLY-LABELLED RNA IN THE MOUSE MAMMARY GLAND BEFORE AND DURING LACTATION

1973 ◽  
Vol 56 (1) ◽  
pp. 145-152 ◽  
Author(s):  
D. N. BANERJEE ◽  
M. R. BANERJEE
Keyword(s):  
Mammary Gland ◽  
Ribosomal Rna ◽  
Gradient Analysis ◽  
Sucrose Density Gradient ◽  
Mouse Mammary Gland ◽  
Nuclear Fraction ◽  
Cytoplasmic Rna ◽  
Nuclear Rna ◽  
Nuclear Synthesis

SUMMARY Linear sucrose density gradient analysis showed that the synthesis of rapidly-labelled high molecular weight RNA was virtually absent in the mammary glands of virgin mice. The rapidly-labelled RNA was first evident in the mammary gland in pregnancy and was also present during lactation. The bulk of this newly-made nuclear RNA sedimented as 45S and 32S fractions after a 15-min [3H]uridine pulse period in vivo. No labelled 18S RNA was detectable in the nuclear fraction after the 15-min pulse but it was present in the cytoplasm, suggesting that the 18S RNA migrates to the cytoplasm almost immediately after its formation. Thirty minutes after injection of [3H]uridine, the initial radioactivity of the 45S region migrated to the 32S fraction and a labelled 28S peak was also present in the cytoplasmic RNA at 60 min, suggesting that the processed 28S ribosomal RNA in the mammary gland began to migrate to the cytoplasm between 30 and 60 min after the nuclear synthesis of the precursor molecule.

scholarly journals The p53 tumor suppressor gene is regulated in vivo by nuclear factor 1-C2 in the mouse mammary gland during pregnancy

Oncogene ◽  
2003 ◽  
Vol 22 (38) ◽  
pp. 6061-6070 ◽  
Author(s):  
Eva M Johansson ◽  
Marie Kannius-Janson ◽  
Gunnar Bjursell ◽  
Jeanette Nilsson
Keyword(s):  
Mammary Gland ◽  
Tumor Suppressor ◽  
Tumor Suppressor Gene ◽  
Suppressor Gene ◽  
Mouse Mammary Gland ◽  
Nuclear Factor ◽  
P53 Tumor Suppressor ◽  
P53 Tumor Suppressor Gene ◽  
Nuclear Factor 1

scholarly journals Developmental regulation of Bcl-2 family protein expression in the involuting mammary gland

1999 ◽  
Vol 112 (11) ◽  
pp. 1771-1783 ◽  
Author(s):  
A.D. Metcalfe ◽  
A. Gilmore ◽  
T. Klinowska ◽  
J. Oliver ◽  
A.J. Valentijn ◽  
...  
Keyword(s):  
Cell Death ◽  
Mammary Gland ◽  
Epithelial Cells ◽  
De Novo ◽  
Mammary Epithelial Cells ◽  
Expression Profiles ◽  
Mammary Epithelial ◽  
Mammary Tissue ◽  
Pregnancy And Lactation

Epithelial cells within the mammary gland undergo developmental programmes of proliferation and apoptosis during the pregnancy cycle. After weaning, secretory epithelial cells are removed by apoptosis. To determine whether members of the Bcl-2 gene family could be involved in regulating this process, we have examined whether changes in their expression occur during this developmental apoptotic program in vivo. Bax and Bcl-x were evenly expressed throughout development. However, expression of Bak and Bad was increased during late pregnancy and lactation, and the proteins were present during the time of maximal apoptotic involution. Thereafter, their levels declined. In contrast, Bcl-w was expressed in pregnancy and lactation but was downregulated at the onset of apoptosis. Bcl-2 was not detected in lactating or early involuting mammary gland. Thus, the pro-apoptotic proteins Bax, Bak and Bad, as well as the death-suppressors Bcl-x, Bcl-2 and Bcl-w, are synthesised in mouse mammary gland, and dynamic changes in the expression profiles of these proteins occurs during development. To determine if changes in Bak and Bcl-w expression could regulate mammary apoptosis, their effect on cultured mouse mammary epithelial cells was examined in transient transfection assays. Enforced expression of Bak induced rapid mammary apoptosis, which could be suppressed by coexpression of Bcl-w. In extracts of mammary tissue in vivo, Bak heterodimerized with Bcl-x whereas Bax associated with Bcl-w, but Bak/Bcl-w heterodimers were not detected. Thus, Bak and Bcl-w may regulate cell death through independent pathways. These results support a model in which mammary epithelial cells are primed for apoptosis during the transition from pregnancy to lactation by de novo expression of the death effectors Bak and Bad. It is suggested that these proteins are prevented from triggering apoptosis by anti-apoptotic Bcl-2 family proteins until involution, when the levels of Bcl-w decline. Our study provides evidence that regulated changes in the expression of cell death genes may contribute to the developmental control of mammary apoptosis.

scholarly journals The effect of lipid derivative of anti-tumor drug sarcolysin embedded in phospholipid nanoparticles in the experiments in vivo

2021 ◽  
Vol 67 (6) ◽  
pp. 491-499
Author(s):  
Yu.A. Tereshkina ◽  
T.I. Torkhovskaya ◽  
M.A. Sanzhakov ◽  
L.V. Kostryukova ◽  
Yu.Yu. Khudoklinova ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Antitumor Agent ◽  
Mouse Mammary Gland ◽  
Lymphocytic Leukemia ◽  
Pharmacokinetic Parameters ◽  
Tumor Growth Inhibition ◽  
Phospholipid Nanoparticles ◽  
Lipid Derivative ◽  
Ld50 Value

To improve the therapeutic properties of the antitumor agent Sarcolysin, we have previously developed and characterized a dosage form representing its ester conjugate with decanol embedded in ultra-small phospholipid nanoparticles less than 30 nm in size (“Sarcolysin-NP”). The effect of the resulting composition was investigated in vivo in comparison with the free substance of sarcolysin. The composition intravenous administration to mice showed an improvement in the pharmacokinetic parameters of sarcolysin associated with its initial higher (by 22%) level in the blood and prolonged circulation, which was also observed in mice with P388 tumor. In mice with three types of tumors — lymphocytic leukemia P388, lymphocytic leukemia L1210, and adenocarcinoma of the mammary gland Ca755 — administration of two doses of sarcolysin over a period of 7 days showed its predominant antitumor effect. The maximum tumor growth inhibition was noted for lymphocytic leukemia L1210 and adenocarcinoma of the mouse mammary gland Ca755 (at a dose of Sarcolysin-NP — 8,4 mg/kg), which was higher in comparison with free substance by more than 24% and 17%, respectively. Differences in the life span of the treated animals were revealed significantly at a dose of 10 mg/kg and amounted to 25% and 17,4% for lymphocytic leukemia P388 and L1210, respectively, and 11% for adenocarcinoma Ca755. In an experiment on rats, acute toxicity of Sarcolysin-NP administered intravenously showed that an average LD50 value 2-3 times exceeded a similar parameter for commercial preparations of free sarcolysin (Melphalan and Alkeran), which indicates its lower toxicity.

Electrical potentials and cell-to-cell dye movement in mouse mammary gland during lactation

1984 ◽  
Vol 247 (1) ◽  
pp. C20-C25 ◽  
Author(s):  
S. E. Berga
Keyword(s):  
Mammary Gland ◽  
Lucifer Yellow ◽  
Mammary Epithelium ◽  
Mouse Mammary Gland ◽  
Dye Transfer ◽  
Alveolar Cells ◽  
Electrical Potentials ◽  
Lucifer Yellow Ch ◽  
Electrophysiological Studies

Stable potentials were recorded with microelectrodes in an in vivo preparation of the mammary gland from the anesthetized lactating mouse. Location of the microelectrode tip was determined by ionophoretic injection of the fluorescent dye Lucifer yellow CH. Fifteen dye injections were localized to mammary alveolar cells; the average recorded potential for these penetrations was -49 +/- 2 mV. Cell-to-cell dye transfer between alveolar cells was observed with all intracellular Lucifer yellow injections. Ten dye injections were localized to the alveolar lumina with an average recorded potential of -35 +/- 2 mV. With these penetrations Lucifer yellow spread rapidly to many alveolar lumina. These findings indicate that stable potentials can be obtained from both cells and lumina in the in vivo mammary gland, demonstrating the feasibility of electrophysiological studies of the mammary epithelium. The presence of a large transepithelial potential provides evidence for physiologically tight junctions between mammary alveolar cells. In addition, the distribution of Lucifer yellow shows that mammary alveolar cells are coupled and suggests that milk flows freely between alveolar lumina.

Role for Tyrosine Phosphorylation and Lyn Tyrosine Kinase in Fas Receptor-Mediated Apoptosis in Eosinophils

Blood ◽  
1998 ◽  
Vol 92 (2) ◽  
pp. 547-557 ◽  
Author(s):  
Hans-Uwe Simon ◽  
Shida Yousefi ◽  
Birgit Dibbert ◽  
Holger Hebestreit ◽  
Martina Weber ◽  
...  
Keyword(s):  
Cell Death ◽  
Tyrosine Kinase ◽  
Tyrosine Phosphorylation ◽  
Tyrosine Kinases ◽  
Fas Ligand ◽  
In Vivo Model ◽  
Fas Receptor ◽  
Human And Mouse

Fas ligand/Fas receptor molecular interactions have been implicated as having an important function for the regulation of eosinophil apoptosis. The purpose of the present study was to investigate biochemical events triggered by the engagement of the Fas receptor in freshly isolated human and mouse eosinophils. Activation of the Fas receptor on eosinophils with the agonistic anti-Fas monoclonal antibody (MoAb) resulted in increased tyrosine phosphorylation of several intracellular proteins. The tyrosine kinase inhibitors lavendustin A and genistein inhibited Fas receptor-induced cell death in both human and mouse eosinophils in vitro and prevented, at least partially, Fas receptor-mediated resolution of eosinophilic inflammation in a mouse in vivo model of lung eosinophilia. In addition, in freshly purified human eosinophils, lavendustin A prevented anti-Fas MoAb-induced proteolytic cleavage of lamin B, suggesting that tyrosine kinases may amplify the proteolytic signaling cascade within interleukin-1β converting enzyme (ICE) family proteases. Moreover, the tyrosine kinase Lyn was identified as being involved in Fas receptor-mediated cell death. Collectively, these results demonstrate that tyrosine phosphorylation is an important step in the generation of the Fas receptor-linked transmembrane death signal in eosinophils and that Lyn participates in this pathway.

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