Document Detail


Non-human primate fetal kidney transcriptome analysis indicates mammalian target of rapamycin (mTOR) is a central nutrient-responsive pathway.
MedLine Citation:
PMID:  17185341     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Developmental programming is defined as the process by which gene-environment interaction in the developing organism leads to permanent changes in phenotype and function. Numerous reports of maternal nutrient restriction during pregnancy demonstrate altered renal development. Typically this alteration manifests as a reduction in the total number of glomeruli in the mature kidney of the offspring, and suggests that predisposition to develop chronic renal disease may include an in utero origin. In a previous study, we defined the transcriptome in the kidney from fetuses of control (CON, fed ad libitum) and nutrient-restricted (NR, fed 70% of CON starting at 0.16 gestation (G)) pregnancies at half-way through gestation (0.5G), and established transcriptome and morphological changes in NR kidneys compared to CON. One goal of the present study was to use transcriptome data from fetal kidneys of CON and NR mothers at 0.5G with histological data to identify the molecular mechanisms that may regulate renal development. A second goal was to identify mechanisms by which NR elicits its affect on fetal baboon kidney. We have used an end-of-pathway gene expression analysis to prioritize and identify key pathways regulating the 0.5G kidney phenotype in response NR. From these data we have determined that the mammalian target of rapamycin (mTOR) signalling pathway is central to this phenotype.
Authors:
Mark J Nijland; Natalia E Schlabritz-Loutsevitch; Gene B Hubbard; Peter W Nathanielsz; Laura A Cox
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2006-12-21
Journal Detail:
Title:  The Journal of physiology     Volume:  579     ISSN:  0022-3751     ISO Abbreviation:  J. Physiol. (Lond.)     Publication Date:  2007 Mar 
Date Detail:
Created Date:  2007-03-16     Completed Date:  2007-05-16     Revised Date:  2013-09-02    
Medline Journal Info:
Nlm Unique ID:  0266262     Medline TA:  J Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  643-56     Citation Subset:  IM    
Affiliation:
Department of Obstetrics and Gynecology and Center for Pregnancy and Newborn Research, University of Texas Health Science Center, San Antonio, TX, USA.
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MeSH Terms
Descriptor/Qualifier:
Animal Feed
Animal Nutritional Physiological Phenomena / genetics
Animals
Caloric Restriction
Female
Gene Expression Regulation, Developmental*
Genomics
Immunohistochemistry
Kidney / embryology*,  physiology*
Maternal Nutritional Physiological Phenomena / genetics*
Papio
Phenotype
Pregnancy
Protein Kinases / genetics*,  metabolism
Signal Transduction / genetics
TOR Serine-Threonine Kinases
Transcription, Genetic
Vascular Endothelial Growth Factor A / genetics,  metabolism
Grant Support
ID/Acronym/Agency:
1 C06 RR13556/RR/NCRR NIH HHS; HD21350/HD/NICHD NIH HHS; P01 HD021350/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Vascular Endothelial Growth Factor A; EC 2.7.-/Protein Kinases; EC 2.7.1.1/MTOR protein, human; EC 2.7.1.1/TOR Serine-Threonine Kinases
Comments/Corrections

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