Programmed cell death and the mammary gland - The involvement of the Bcl-2 family members in the control of epithelial apoptosis

1996 ◽  
Vol 24 (3) ◽  
pp. 347S-347S ◽  
Author(s):  
Anthony D. Metcalfe ◽  
John A. Hickman ◽  
Charles H. Streuli
Keyword(s):  
Cell Death ◽  
Mammary Gland ◽  
Programmed Cell Death ◽  
Family Members

scholarly journals Hormonal control of programmed cell death/apoptosis

1998 ◽  
pp. 482-491 ◽  
Author(s):  
W Kiess ◽  
B Gallaher
Keyword(s):  
Cell Death ◽  
Mammary Gland ◽  
Growth Factors ◽  
Growth Factor ◽  
Programmed Cell Death ◽  
Cell Types ◽  
Hormonal Control ◽  
Endocrine Glands ◽  
Survival Factors ◽  
Endocrine Tissues

Apoptosis or programmed cell death is a physiological form of cell death that occurs in embryonic development and during involution of organs. It is characterized by distinct biochemical and morphological changes such as DNA fragmentation, plasma membrane blebbing and cell volume shrinkage. Many hormones, cytokines and growth factors are known to act as general and/or tissue-specific survival factors preventing the onset of apoptosis. In addition, many hormones and growth factors are also capable of inducing or facilitating programmed cell death under physiological or pathological conditions, or both. Steroid hormones are potent regulators of apoptosis in steroid-dependent cell types and tissues such as the mammary gland, the prostate, the ovary and the testis. Growth factors such as epidermal growth factor, nerve growth factor, platelet-derived growth factor (PDGF) and insulin-like growth factor-I act as survival factors and inhibit apoptosis in a number of cell types such as haematopoietic cells, preovulatory follicles, the mammary gland, phaeochromocytoma cells and neurones. Conversely, apoptosis modulates the functioning and the functional integrity of many endocrine glands and of many cells that are capable of synthesizing and secreting hormones. In addition, exaggeration of the primarily natural process of apoptosis has a key role in the pathogenesis of diseases involving endocrine tissues. Most importantly, in autoimmune diseases such as autoimmune thyroid disease and type 1 diabetes mellitus, new data suggest that the immune system itself may not carry the final act of organ injury: rather, the target cells (i.e. thyrocytes and beta cells of the islets) commit suicide through apoptosis. The understanding of how hormones influence programmed cell death and, conversely, of how apoptosis affects endocrine glands, is central to further design strategies to prevent and treat diseases that affect endocrine tissues. This short review summarizes the available evidence showing where and how hormones control apoptosis and where and how programmed cell death exerts modulating effects upon hormonally active tissues.

Differential regulation of transcription and induction of programmed cell death by human p53-family members p63 and p73

FEBS Letters ◽  
2002 ◽  
Vol 525 (1-3) ◽  
pp. 93-99 ◽  
Author(s):  
Sebastian Dietz ◽  
Karen Rother ◽  
Casimir Bamberger ◽  
Hartwig Schmale ◽  
Joachim Mössner ◽  
...  
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Family Members ◽  
Differential Regulation ◽  
Regulation Of Transcription ◽  
P53 Family

BH3-only proteins — evolutionarily conserved proapoptotic Bcl-2 family members essential for initiating programmed cell death

2002 ◽  
Vol 115 (8) ◽  
pp. 1567-1574 ◽  
Author(s):  
Philippe Bouillet ◽  
Andreas Strasser
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Family Members ◽  
Protein Family ◽  
Cell Stress ◽  
Protective Function ◽  
Evolutionarily Conserved ◽  
Apoptotic Cascade

The BH3-only members of the Bcl-2 protein family are essential initiators of programmed cell death and are required for apoptosis induced by cytotoxic stimuli. These proteins have evolved to recognise distinct forms of cell stress. In response, they unleash the apoptotic cascade by inactivating the protective function of the pro-survival members of the Bcl-2 family and by activating the Bax/Bax-like pro-apoptotic family members.

scholarly journals Effect of Staphylococcus aureus and Streptococcus uberis on apoptosis of bovine mammary gland neutrophils in vitro

2012 ◽  
Vol 50 (No. 1) ◽  
pp. 11-23 ◽  
Author(s):  
Z. Sladek ◽  
D. Rysanek ◽  
M. Faldyna
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Death ◽  
Mammary Gland ◽  
Programmed Cell Death ◽  
Propidium Iodide ◽  
Annexin V ◽  
Dna Fragments ◽  
Bovine Mammary Gland ◽  
Streptococcus Uberis

Neutrophils play an important role in the defence of the bovine mammary gland against bacterial infections. In the course of the resolution of mammary gland inflammation, neutrophils undergo programmed cell death – apoptosis. The aim of this study was to confirm whether the co-cultivation of neutrophils of the bovine mammary gland with either Staphylococcus aureus or Streptococcus uberis leads to signs of apoptosis. In the study, 16 mammary glands of four virgin heifers aged 16 to 18 months were examined. Neutrophils were obtained by lavage after an induced influx. After a three-hour incubation of the neutrophils with bacteria in vitro, neutrophil apoptosis was detected by morphological features, by determination of histone-associated DNA fragments (ELISA), and by Annexin -V and propidium iodide positivity (flow cytometry). S. aureus and S. uberis reduced the incidence of karyopycnotic and zeiotic neutrophils (P < 0.01), and insignificantly reduced the concentration of histone -associated DNA fragments (P > 0.05). The incubation of neutrophils with bacteria, however, increased the proportion of Annexin –V-positive cells (P < 0.01) and Annexin -V and propidium iodide-positive cells (P < 0.05). Co-cultivation of neutrophils with either S. aureus or S. uberis led to the induction of phosphatidylserine translocation characteristic of the early stage of apoptosis. The late signs of apoptosis were delayed by co-cultivation of neutrophils with both pathogens. Therefore it is obvious that although the programmed cell death of apoptosis is initiated by these pathogens, the completion of the program is delayed.

scholarly journals Glucocorticoid and progesterone inhibit involution and programmed cell death in the mouse mammary gland.

1995 ◽  
Vol 131 (4) ◽  
pp. 1095-1103 ◽  
Author(s):  
Z Feng ◽  
A Marti ◽  
B Jehn ◽  
H J Altermatt ◽  
G Chicaiza ◽  
...  
Keyword(s):  
Cell Death ◽  
Mammary Gland ◽  
Programmed Cell Death ◽  
Hormone Receptors ◽  
Target Genes ◽  
Mouse Mammary Gland ◽  
Binding Activity ◽  
Steroid Hormone Receptors ◽  
Mrna Levels ◽  
Glucocorticoid Hormone

Milk production during lactation is a consequence of the suckling stimulus and the presence of glucocorticoids, prolactin, and insulin. After weaning the glucocorticoid hormone level drops, secretory mammary epithelial cells die by programmed cell death and the gland is prepared for a new pregnancy. We studied the role of steroid hormones and prolactin on the mammary gland structure, milk protein synthesis, and on programmed cell death. Slow-release plastic pellets containing individual hormones were implanted into a single mammary gland at lactation. At the same time the pups were removed and the consequences of the release of hormones were investigated histologically and biochemically. We found a local inhibition of involution in the vicinity of deoxycorticosterone- and progesterone-release pellets while prolactin-release pellets were ineffective. Dexamethasone, a very stable and potent glucocorticoid hormone analogue, inhibited involution and programmed cell death in all the mammary glands. It led to an accumulation of milk in the glands and was accompanied by an induction of protein kinase A, AP-1 DNA binding activity and elevated c-fos, junB, and junD mRNA levels. Several potential target genes of AP-1 such as stromelysin-1, c-jun, and SGP-2 that are induced during normal involution were strongly inhibited in dexamethasone-treated animals. Our results suggest that the cross-talk between steroid hormone receptors and AP-1 previously described in cells in culture leads to an impairment of AP-1 activity and to an inhibition of involution in the mammary gland implying that programmed cell death in the postlactational mammary gland depends on functional AP-1.

Differential functions of calpain 1 during epithelial cell death and adipocyte differentiation in mammary gland involution

2014 ◽  
Vol 459 (2) ◽  
pp. 355-368 ◽  
Author(s):  
Teresa Arnandis ◽  
Ivan Ferrer-Vicens ◽  
Luis Torres ◽  
Concha García ◽  
Elena R. Garcia-Trevijano ◽  
...  
Keyword(s):  
Cell Death ◽  
Mammary Gland ◽  
Epithelial Cell ◽  
Programmed Cell Death ◽  
Adipocyte Differentiation ◽  
Histone H3 ◽  
Tissue Remodelling ◽  
Mammary Gland Involution ◽  
Epithelial Cell Death

The results of the present study unveil novel and important nuclear functions of calpains in tissue remodelling. Although inducing nuclear permeability during programmed cell death, histone H3 is identified as a new target of calpain-1 upon adipocyte differentiation.

Promoter cloning and characterization of the human programmed cell death protein 4 (pdcd4) gene: evidence for ZBP-89 and Sp-binding motifs as essential Pdcd4 regulators

2012 ◽  
Vol 32 (3) ◽  
pp. 281-297 ◽  
Author(s):  
Jörg Hendrik Leupold ◽  
Irfan Ahmed Asangani ◽  
Giridhar Mudduluru ◽  
Heike Allgayer
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Promoter Activity ◽  
Family Members ◽  
Tumour Suppressor ◽  
Solid Cancer ◽  
Basal Region ◽  
Mobility Shift ◽  
Basal Promoter Activity ◽  
Cell Death Protein

Pdcd4 (programmed cell death protein 4) is an important novel tumour suppressor inhibiting transformation, translation, invasion and intravasation, and its expression is down-regulated in several cancers. However, little is known about the transcriptional regulation and the promoter of this important tumour suppressor. So far the following is the first comprehensive study to describe the regulation of Pdcd4 transcription by ZBP-89 (zinc-finger-binding protein 89), besides characterizing the gene promoter. We identified the transcriptional start sites of the human pdcd4 promoter, a functional CCAAT-box, and the basal promoter region. Within this basal region, computer-based analysis revealed several potential binding sites for ZBPs, especially for Sp (specificity protein) family members and ZBP-89. We identified four Sp1/Sp3/Sp4-binding elements to be indispensable for basal promoter activity. However, overexpression of Sp1 and Sp3 was not sufficient to enhance Pdcd4 protein expression. Analysis in different solid cancer cell lines showed a significant correlation between pdcd4 and zbp-89 mRNA amounts. In contrast with Sp transcription factors, overexpression of ZBP-89 led to an enhanced expression of Pdcd4 mRNA and protein. Additionally, specific knockdown of ZBP-89 resulted in a decreased pdcd4 gene expression. Reporter gene analysis showed a significant up-regulation of basal promoter activity by co-transfection with ZBP-89, which could be abolished by mithramycin treatment. Predicted binding of ZBP-89 to the basal promoter was confirmed by EMSA (electrophoretic mobility-shift assay) data and supershift analysis for ZBP-89. Taken together, data for the first time implicate ZBP-89 as a regulator of Pdcd4 by binding to the basal promoter either alone or by interacting with Sp family members.

ROLE OF BH3-ONLY PRO-APOPTOTIC BCL-2 FAMILY MEMBERS IN PROGRAMMED CELL DEATH AND PATHOLOGY

Shock ◽  
2004 ◽  
Vol 21 (Supplement) ◽  
pp. 53
Author(s):  
A Strasser ◽  
P. Bouillet ◽  
A. Villunger ◽  
L Coultas ◽  
E Michalak
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Family Members

scholarly journals Plant and animal PR1 family members inhibit programmed cell death and suppress bacterial pathogens in plant tissues

2018 ◽  
Vol 19 (9) ◽  
pp. 2111-2123 ◽  
Author(s):  
James E. Lincoln ◽  
Juan P. Sanchez ◽  
Kristina Zumstein ◽  
David G. Gilchrist
Keyword(s):  
Cell Death ◽  
Programmed Cell Death ◽  
Bacterial Pathogens ◽  
Family Members ◽  
Plant Tissues
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