Development of a P2X1-purinoceptor mediated contractile response in the aged mouse prostate gland through slowing down of ATP breakdown

2013 ◽  
Vol 34 (3) ◽  
pp. 292-298 ◽  
Author(s):  
Carl W. White ◽  
Jennifer L. Short ◽  
Richard J. Evans ◽  
Sabatino Ventura
Keyword(s):  
Contractile Response ◽  
Prostate Gland ◽  
Aged Mouse ◽  
Slowing Down ◽  
Mouse Prostate ◽  
Atp Breakdown

scholarly journals Estrogen receptor 1 expression and methylation of Esr1 promoter in mouse fetal prostate mesenchymal cells induced by gestational exposure to bisphenol A or ethinylestradiol

2019 ◽  
Vol 5 (3) ◽  
Author(s):  
Ramji K Bhandari ◽  
Julia A Taylor ◽  
Jennifer Sommerfeld-Sager ◽  
Donald E Tillitt ◽  
William A Ricke ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Bisphenol A ◽  
Oral Contraceptives ◽  
Primary Cultures ◽  
Prostate Gland ◽  
Mesenchymal Cells ◽  
Urogenital Sinus ◽  
Environmental Estrogen ◽  
Mouse Prostate

Abstract Fetal/neonatal environmental estrogen exposures alter developmental programing of the prostate gland causing onset of diseases later in life. We have previously shown in vitro that exposures to 17β-estradiol (E2) and the endocrine disrupting chemical bisphenol A, at concentrations relevant to human exposure, cause an elevation of estrogen receptor α (Esr1) mRNA in primary cultures of fetal mouse prostate mesenchymal cells; a similar result was observed in the fetal rat urogenital sinus. Effects of these chemicals on prostate mesenchyme in vivo are not well understood. Here we show effects in mice of fetal exposure to the estrogenic drug in mixed oral contraceptives, 17α-ethinylestradiol (EE2), at a concentration of EE2 encountered by human embryos/fetuses whose mothers become pregnant while on EE2-containing oral contraceptives, or bisphenol A at a concentration relevant to exposures observed in human fetuses in vivo. Expression of Esr1 was elevated by bisphenol A or EE2 exposures, which decreased the global expression of DNA methyltransferase 3A (Dnmt3a), while methylation of Esr1 promoter was significantly increased. These results show that exposures to the environmental estrogen bisphenol A and drug EE2 cause transcriptional and epigenetic alterations to expression of estrogen receptors in developing prostate mesenchyme in vivo.

scholarly journals Lectin-binding sites in epithelial cells of the mouse prostate gland

2015 ◽  
Vol 91 (4) ◽  
pp. 91-95 ◽  
Author(s):  
Kentaro SAKUDA ◽  
Ayaka YOSHIDA ◽  
Ryoki MURAGISHI ◽  
Kazuya YOSHINAGA
Keyword(s):  
Epithelial Cells ◽  
Binding Sites ◽  
Lectin Binding ◽  
Prostate Gland ◽  
Mouse Prostate ◽  
Lectin Binding Sites

EFFECTS OF A SINGLE INJECTION OF TESTOSTERONE AND/OR ETHINYLOESTRADIOL UPON MOUSE PROSTATE GLAND FRUCTOSE LEVELS

1969 ◽  
Vol 62 (2) ◽  
pp. 319-327 ◽  
Author(s):  
J. A. Thomas ◽  
M. Mawhinney ◽  
E. T. Knych
Keyword(s):  
Membrane Permeability ◽  
Single Injection ◽  
Prostate Gland ◽  
Target Organ ◽  
Stimulatory Action ◽  
Early Stimulation ◽  
Hormone Administration ◽  
Mouse Prostate ◽  
Higher Doses ◽  
Stimulation Of

ABSTRACT Single injections of testosterone (20 mg/kg) to castrated mice caused an early stimulation in TCA-extractable fructose. Later, and at somewhat higher doses, free fructose levels were observed to rise. The earliest detectable changes occurred about 12 h following injection. Single injections of ethinyloestradiol to recently castrated mice (48 h) caused a stimulation of prostate gland TCA-extractable fructose 12 h after hormone administration. Free fructose in these same organs was generally reduced by the administration of this oestrogen. Ethinyloestradiol given one hour prior to a fructose stimulating dose of testosterone produced essentially the same stimulatory response as ethinyloestradiol alone. The stimulatory action of ethinyloestradiol is probably related to changes in membrane permeability in the target organ.

Genetically defined mouse models that mimic natural aspects of human prostate cancer development.

2004 ◽  
Vol 11 (2) ◽  
pp. 225-254 ◽  
Author(s):  
P Roy-Burman ◽  
H Wu ◽  
W C Powell ◽  
J Hagenkord ◽  
M B Cohen
Keyword(s):  
Prostate Cancer ◽  
Mouse Models ◽  
Prostate Gland ◽  
Genetic Alterations ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Preneoplastic Lesions ◽  
Invasive Adenocarcinoma ◽  
Mouse Prostate ◽  
Genetically Manipulated

This review is focused on mouse models for prostate cancer that have been designed on the basis of genetic alterations that are frequently found in human prostate cancer. It begins with an analysis of the similarities and differences in the gross and microscopic anatomy of the mouse and human prostate glands, and extends to the pathologies induced in the genetically manipulated mouse prostate in comparison with the sporadic development of the disease in humans. Major achievements have been made in modeling human prostate cancer in mice in recent years. There are models which display slow, temporal development of increasingly severe preneoplastic lesions, which are remarkably restricted to the prostate gland, a property similar to the aging-related progression of these lesions in humans. Other models rapidly progress to local invasive adenocarcinoma, and, in some of them metastasis is manifested subsequently with defined kinetics. Global assessment of molecular changes in the prostate of the genetically manipulated mice is increasingly underscoring the validity of the models through identification of 'signature' genes which are associated with the organ-confined primary or distant metastases of human prostate cancer. Taken together, various 'natural' models depicting stages of the disease, ranging from the early preneoplastic lesions to metastatic prostate cancer, now provide new tools both for exploring the molecular mechanism underlying prostate cancer and for development or testing of new targeted therapies.

scholarly journals A luciferase transgenic mouse model: visualization of prostate development and its androgen responsiveness in live animals

2005 ◽  
Vol 35 (2) ◽  
pp. 293-304 ◽  
Author(s):  
C-L Hsieh ◽  
Z Xie ◽  
Z-Y Liu ◽  
J E Green ◽  
W D Martin ◽  
...  
Keyword(s):  
Mouse Model ◽  
Luciferase Activity ◽  
Prostate Gland ◽  
Specific Antigen ◽  
Firefly Luciferase ◽  
Prostate Development ◽  
Highly Active ◽  
Mouse Prostate ◽  
Imaging Results ◽  
High Level

Numerous mouse models of prostate carcinogenesis have been developed, but hitherto there has been no model in which the prostate gland could be imaged in live animals. The transgenic model generated here targeted mouse prostate gland using a firefly luciferase enzyme under the control of a small but highly active and specific supra prostate-specific antigen (sPSA) promoter. We evaluated postnatal prostate development, involution and androgen-induced restoration of prostate growth in adult transgenic mice using bioluminescence imaging. Results of our study showed that: (i) the prostate gland of male offspring did not yield a significant bioluminescence signal until after sexual maturity. Luciferase was detected in the luminal epithelial cells of the ventral and dorsolateral lobes of the prostate gland and caput epididymis, with little or no activity in 18 other organs evaluated. (ii) While a constant high level of bioluminescence was detected in the mouse prostate from 5 to 35 weeks of age, a slight drop in bioluminescence was detected at 36 to 54 weeks. (iii) Upon castration, the luciferase activity signal associated with mouse prostate detected by a cooled charge-coupled device camera was dramatically reduced. This signal could be rapidly restored to pre-castration levels after androgen administration. Androgen-induced luciferase activity subsided to nearly basal levels 5 days following the last injection. These data demonstrate that a bioluminescent mouse model with luciferase activity restricted to the prostate gland under the control of a (sPSA) promoter can be used on a real-time basis in live animals to investigate the development and responsiveness of the prostate gland to exogenously administered androgen. This model can be extended to detect the responsiveness of the prostate gland to therapy and used as a founder strain to visualize tumors in hosts with different genetic backgrounds.

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