PMID- 17185341
OWN - NLM
STAT- MEDLINE
DCOM- 20070516
LR  - 20211203
IS  - 0022-3751 (Print)
IS  - 1469-7793 (Electronic)
IS  - 0022-3751 (Linking)
VI  - 579
IP  - Pt 3
DP  - 2007 Mar 15
TI  - Non-human primate fetal kidney transcriptome analysis indicates mammalian target 
      of rapamycin (mTOR) is a central nutrient-responsive pathway.
PG  - 643-56
AB  - 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.
FAU - Nijland, Mark J
AU  - Nijland MJ
AD  - Department of Obstetrics and Gynecology and Center for Pregnancy and Newborn 
      Research, University of Texas Health Science Center, San Antonio, TX, USA.
FAU - Schlabritz-Loutsevitch, Natalia E
AU  - Schlabritz-Loutsevitch NE
FAU - Hubbard, Gene B
AU  - Hubbard GB
FAU - Nathanielsz, Peter W
AU  - Nathanielsz PW
FAU - Cox, Laura A
AU  - Cox LA
LA  - eng
GR  - C06 RR013556/RR/NCRR NIH HHS/United States
GR  - P01 HD021350/HD/NICHD NIH HHS/United States
GR  - 1 C06 RR13556/RR/NCRR NIH HHS/United States
GR  - HD21350/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20061221
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 2.7.1.1 (MTOR protein, human)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Animal Feed
MH  - Animal Nutritional Physiological Phenomena/genetics
MH  - Animals
MH  - Caloric Restriction
MH  - Female
MH  - *Gene Expression Regulation, Developmental
MH  - Genomics
MH  - Immunohistochemistry
MH  - Kidney/*embryology/*physiology
MH  - Maternal Nutritional Physiological Phenomena/*genetics
MH  - Papio
MH  - Phenotype
MH  - Pregnancy
MH  - Protein Kinases/*genetics/metabolism
MH  - Signal Transduction/genetics
MH  - TOR Serine-Threonine Kinases
MH  - Transcription, Genetic
MH  - Vascular Endothelial Growth Factor A/genetics/metabolism
PMC - PMC2151384
EDAT- 2006/12/23 09:00
MHDA- 2007/05/17 09:00
PMCR- 2008/03/15
CRDT- 2006/12/23 09:00
PHST- 2006/12/23 09:00 [pubmed]
PHST- 2007/05/17 09:00 [medline]
PHST- 2006/12/23 09:00 [entrez]
PHST- 2008/03/15 00:00 [pmc-release]
AID - jphysiol.2006.122101 [pii]
AID - 10.1113/jphysiol.2006.122101 [doi]
PST - ppublish
SO  - J Physiol. 2007 Mar 15;579(Pt 3):643-56. doi: 10.1113/jphysiol.2006.122101. Epub 
      2006 Dec 21.