Document Detail


Overactivation of hedgehog signaling alters development of the ovarian vasculature in mice.
MedLine Citation:
PMID:  22402963     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The hedgehog (HH) signaling pathway is critical for ovarian function in Drosophila, but its role in the mammalian ovary has not been defined. Previously, expression of a dominant active allele of the HH signal transducer protein smoothened (SMO) in Amhr2(cre/+)SmoM2 mice caused anovulation in association with a lack of smooth muscle in the theca of developing follicles. The current study examined events during the first 2 wk of life in Amhr2(cre/+)SmoM2 mice to gain insight into the cause of anovulation. Expression of transcriptional targets of HH signaling, Gli1, Ptch1, and Hhip, which are used as measures of pathway activity, were elevated during the first several days of life in Amhr2(cre/+)SmoM2 mice compared to controls but were similar to controls in older mice. Microarray analysis showed that genes with increased expression in 2-day-old mutants compared to controls were enriched for the processes of vascular and tube development and steroidogenesis. The density of platelet endothelial cell adhesion molecule (PECAM)-labeled endothelial tubes was increased in the cortex of newborn ovaries of mutant mice. Costaining of preovulatory follicles for PECAM and smooth muscle actin showed that muscle-type vascular support cells are deficient in theca of mutant mice. Expression of genes for steroidogenic enzymes that are normally expressed in the fetal adrenal gland were elevated in newborn ovaries of mutant mice. In summary, overactivation of HH signaling during early life alters gene expression and vascular development and this is associated with the lifelong development of anovulatory follicles in which the thecal vasculature fails to mature appropriately.
Authors:
Yi Ren; Robert G Cowan; Fernando F Migone; Susan M Quirk
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2012-06-07
Journal Detail:
Title:  Biology of reproduction     Volume:  86     ISSN:  1529-7268     ISO Abbreviation:  Biol. Reprod.     Publication Date:  2012 Jun 
Date Detail:
Created Date:  2012-06-08     Completed Date:  2012-10-16     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  0207224     Medline TA:  Biol Reprod     Country:  United States    
Other Details:
Languages:  eng     Pagination:  174     Citation Subset:  IM    
Affiliation:
Department of Animal Science, Cornell University, Ithaca, New York 14853, USA.
Data Bank Information
Bank Name/Acc. No.:
GEO/GSE35123
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MeSH Terms
Descriptor/Qualifier:
Animals
Anovulation / congenital
Capillaries / anatomy & histology
Female
Gene Expression Profiling
Gonadal Steroid Hormones / biosynthesis
Hedgehog Proteins / metabolism*
Mice
Muscle, Smooth / anatomy & histology
Mutation
Oligonucleotide Array Sequence Analysis
Ovary / blood supply*,  metabolism,  physiology
Phenotype
Receptors, G-Protein-Coupled / metabolism
Grant Support
ID/Acronym/Agency:
R03HD057648/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Gonadal Steroid Hormones; 0/Hedgehog Proteins; 0/Receptors, G-Protein-Coupled; 0/Smo protein, mouse
Comments/Corrections
Comment In:
Biol Reprod. 2012 Jun;86(6):173   [PMID:  22460668 ]

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