Document Detail


Prepubertal primordial follicle loss in mice is not due to classical apoptotic pathways.
MedLine Citation:
PMID:  19264701     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
More than half of the primordial follicles that are formed by Day 6 of postnatal life in the mouse will be eliminated from the ovary by the time of puberty. Apoptosis, a form of programmed cell death, is one mechanism by which these follicles could be actively lost. To investigate whether apoptosis is responsible for the loss of primordial follicles, follicular atresia was examined during the prepubertal period, when follicles die and are cleared from the ovary at an extremely high rate. Four hallmarks of classical apoptosis were measured in follicles present in prepubertal ovaries. The primordial follicle cohort was not positively associated with nuclear condensation or cell shrinkage, activation of caspase 3, cleavage of poly(ADP ribose) polymerase 1 (PARP1), or fragmentation of DNA. These data are consistent with a nonapoptotic pathway that is responsible for small follicle death.
Authors:
Candace M Tingen; Sarah K Bristol-Gould; Sarah E Kiesewetter; Jason Tyler Wellington; Lonnie Shea; Teresa K Woodruff
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-03-04
Journal Detail:
Title:  Biology of reproduction     Volume:  81     ISSN:  0006-3363     ISO Abbreviation:  Biol. Reprod.     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-26     Completed Date:  2009-09-22     Revised Date:  2011-07-28    
Medline Journal Info:
Nlm Unique ID:  0207224     Medline TA:  Biol Reprod     Country:  United States    
Other Details:
Languages:  eng     Pagination:  16-25     Citation Subset:  IM    
Affiliation:
Department of Obstetrics and Gynecology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology*
Caspases / metabolism
Cell Count / methods
Cell Death
Female
Mice
Models, Biological
Models, Theoretical
Ovarian Follicle / cytology,  metabolism,  physiology*
Sexual Maturation / physiology*
Signal Transduction / physiology
Grant Support
ID/Acronym/Agency:
P01 HD 21921/HD/NICHD NIH HHS; P01 HD021921-209001/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
EC 3.4.22.-/Caspases
Comments/Corrections

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