A novel PSMA/GCPII-deficient mouse model shows enlarged seminal vesicles upon aging
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388963%3A_____%2F19%3A00501452" target="_blank" >RIV/61388963:_____/19:00501452 - isvavai.cz</a>
Alternative codes found
RIV/00064203:_____/19:10386514 RIV/68378050:_____/19:00501452 RIV/00216208:11110/19:10386514 RIV/00216208:11130/19:10386514 and 2 more
Result on the web
<a href="https://onlinelibrary.wiley.com/doi/abs/10.1002/pros.23717" target="_blank" >https://onlinelibrary.wiley.com/doi/abs/10.1002/pros.23717</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1002/pros.23717" target="_blank" >10.1002/pros.23717</a>
Alternative languages
Result language
angličtina
Original language name
A novel PSMA/GCPII-deficient mouse model shows enlarged seminal vesicles upon aging
Original language description
Background: Prostate-specific membrane antigen (PSMA), also known as glutamate carboxypeptidase II (GCPII), is an important diagnostic and therapeutic target in prostate cancer. PSMA/GCPII is also expressed in many healthy tissues, but its function has only been established in the brain and small intestine. Several research groups have attempted to produce PSMA/GCPII-deficient mice to study the physiological role of PSMA/GCPII in detail. The outcomes of these studies differ dramatically, ranging from embryonic lethality to production of viable PSMA/GCPII-deficient mice without any obvious phenotype. Methods: We produced PSMA/GCPII-deficient mice (hereafter also referred as Folh1(-/-) mice) by TALEN-mediated mutagenesis on a C57BL/6NCrl background. Using Western blot and an enzyme activity assay, we confirmed the absence of PSMA/GCPII in our Folh1(-/-) mice. We performed anatomical and histopathological examination of selected tissues with a focus on urogenital system. We also examined the PSMA/GCPII expression profile within the mouse urogenital system using an enzyme activity assay and confirmed the presence of PSMA/GCPII in selected tissues by immunohistochemistry. Results: Our Folh1(-/-) mice are viable, breed normally, and do not show any obvious phenotype. Nevertheless, aged Folh1(-/-) mice of 69-72 weeks exhibit seminal vesicle dilation, which is caused by accumulation of luminal fluid. This phenotype was also observed in Folh1(+/-) mice, the overall difference between our three cohorts (Folh1(-/-), Folh1(+/-), and Folh1(+/+)) was highly significant (P < 0.002). Of all studied tissues of the mouse urogenital system, only the epididymis appeared to have a physiologically relevant level of PSMA/GCPII expression. Additional experiments demonstrated that PSMA/GCPII is also present in the human epididymis. Conclusions: In this study, we provide the first evidence characterizing the reproductive tissue phenotype of PSMA/GCPII-deficient mice. These findings will help lay the groundwork for future studies to reveal PSMA/GCPII function in human reproduction.
Czech name
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Czech description
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Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
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OECD FORD branch
10608 - Biochemistry and molecular biology
Result continuities
Project
<a href="/en/project/LO1302" target="_blank" >LO1302: InterBioMed</a><br>
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2019
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Prostate
ISSN
0270-4137
e-ISSN
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Volume of the periodical
79
Issue of the periodical within the volume
2
Country of publishing house
US - UNITED STATES
Number of pages
14
Pages from-to
126-139
UT code for WoS article
000453562300002
EID of the result in the Scopus database
2-s2.0-85052954730