Document Detail


Exposure to retinoic acid in the neonatal but not adult mouse results in synchronous spermatogenesis.
MedLine Citation:
PMID:  21228214     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Retinoic acid (RA) is required for germ cell differentiation, the regulation of which gives rise to a constant production of mature sperm. In testes from 3-day postpartum (dpp) RARE-hsplacZ mice, periodic regions positive for beta-galactosidase activity were observed along the length of the seminiferous tubules. Periodicity was abolished by treatment of neonates with exogenous RA at 2 dpp. To assess the consequences, 2-dpp mice were treated with RA, and the long- and short-term effects were assessed. Long-term effects of neonatal RA exposure included a delay in the appearance of advanced germ cells and the absence of a spermatogenic wave (synchronous spermatogenesis) in the adult. In contrast, RA exposure in vitamin A-sufficient adults did not result in synchronous spermatogenesis but rather induced apoptosis in a subset of spermatogonia. Shortly after (24 h) neonates were exposed, altered expression of known germ cell differentiation and the (Stra8, Kit, Sycp3, and Rec8) meiosis markers and an increase in the number of STRA8 and SYCP3 immunopositive cells were observed relative to those of vehicle controls. However, 48 and 72 h after exposure, a significant reduction in the number of STRA8 and SYCP3 immunopositive cells occurred. Immunohistochemical analysis of a marker for apoptosis demonstrated neonatal exposure resulted in increased germ cell apoptosis, as observed in the adult. Additionally, RA exposure resulted in increased Cyp26a1 expression of the RA-degrading enzyme. Thus, while RA treatment of neonatal and adult mice resulted in apoptosis of spermatogonia, synchronous spermatogenesis occurred only after neonatal RA exposure.
Authors:
Elizabeth M Snyder; Jeffrey C Davis; Qing Zhou; Ryan Evanoff; Michael D Griswold
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-01-12
Journal Detail:
Title:  Biology of reproduction     Volume:  84     ISSN:  1529-7268     ISO Abbreviation:  Biol. Reprod.     Publication Date:  2011 May 
Date Detail:
Created Date:  2011-04-21     Completed Date:  2011-08-23     Revised Date:  2013-07-02    
Medline Journal Info:
Nlm Unique ID:  0207224     Medline TA:  Biol Reprod     Country:  United States    
Other Details:
Languages:  eng     Pagination:  886-93     Citation Subset:  IM    
Affiliation:
School of Molecular Biosciences, Washington State University, Pullman, WA, USA.
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MeSH Terms
Descriptor/Qualifier:
Aging
Animals
Animals, Newborn
Apoptosis
Biological Markers / metabolism
Cytochrome P-450 Enzyme System / metabolism
Genes, Reporter
Isoenzymes / metabolism
Male
Meiosis
Mice
Mice, Inbred Strains
Mice, Transgenic
Nuclear Proteins / metabolism
Periodicity*
Proteins / metabolism
Response Elements
Seminiferous Tubules / cytology,  growth & development*,  metabolism*
Spermatogenesis*
Spermatogonia / cytology,  metabolism
Tretinoin / physiology*
Grant Support
ID/Acronym/Agency:
HD-10808/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Isoenzymes; 0/Nuclear Proteins; 0/Proteins; 0/Stra8 protein, mouse; 0/Sycp3 protein, mouse; 302-79-4/Tretinoin; 9035-51-2/Cytochrome P-450 Enzyme System; EC 1.14.14.1/retinoic acid 4-hydroxylase
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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