PMID- 22595367
OWN - NLM
STAT- MEDLINE
DCOM- 20121121
LR  - 20211021
IS  - 1879-3185 (Electronic)
IS  - 0300-483X (Print)
IS  - 0300-483X (Linking)
VI  - 299
IP  - 2-3
DP  - 2012 Sep 28
TI  - Developmental cigarette smoke exposure: kidney proteome profile alterations in 
      low birth weight pups.
PG  - 80-9
LID - 10.1016/j.tox.2012.04.015 [doi]
AB  - The Brenner hypothesis states that a congenital reduction in nephron number 
      predisposes to adult-onset hypertension and renal failure. The reduction in 
      nephron number induced by proportionally smaller kidney mass may predispose 
      offspring to glomerular hyperfiltration with maturity onset obesity. 
      Developmental cigarette smoke exposure (CSE) results in intrauterine growth 
      retardation with a predisposition to obesity and cardiovascular disease at 
      maturity. Utilizing a mouse model of 'active' developmental CSE (gestational day 
      [GD] 1-postnatal day [PD] 21; cotinine>50 ng/mL) characterized by persistently 
      smaller offspring with proportionally decreased kidney mass, the present study 
      examined the impact of developmental CSE on the abundance of proteins associated 
      with cellular metabolism in the kidney. Following cessation of CSE on PD21, 
      kidney tissue was collected from CSE and Sham exposed pups for 2D-SDS-PAGE based 
      proteome profiling with statistical analysis by partial least 
      squares-discriminant analysis (PLS-DA) with affected molecular pathways 
      identified by ingenuity pathway analysis. Proteins whose expression in the kidney 
      were affected by developmental CSE belonged to the inflammatory disease, cell to 
      cell signaling/interaction, lipid metabolism, small molecule biochemistry, cell 
      cycle, respiratory disease, nucleic acid and carbohydrate metabolism networks. 
      The present findings indicate that developmental CSE alters the kidney proteome. 
      The companion paper details the liver proteome alterations in the same offspring.
CI  - Copyright (c) 2012 Elsevier Ireland Ltd. All rights reserved.
FAU - Jagadapillai, Rekha
AU  - Jagadapillai R
AD  - Department of Molecular, Cellular, and Craniofacial Biology, ULSD, University of 
      Louisville, Louisville, KY, United States.
FAU - Chen, Jing
AU  - Chen J
FAU - Canales, Lorena
AU  - Canales L
FAU - Birtles, Todd
AU  - Birtles T
FAU - Pisano, M Michele
AU  - Pisano MM
FAU - Neal, Rachel E
AU  - Neal RE
LA  - eng
GR  - P30 ES014443/ES/NIEHS NIH HHS/United States
GR  - P20 GM103453/GM/NIGMS NIH HHS/United States
GR  - R21 DA027466/DA/NIDA NIH HHS/United States
GR  - P20 RR017702/RR/NCRR NIH HHS/United States
GR  - P20 RR/DE-17702/DE/NIDCR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20120515
PL  - Ireland
TA  - Toxicology
JT  - Toxicology
JID - 0361055
SB  - IM
MH  - Animals
MH  - Animals, Newborn
MH  - Discriminant Analysis
MH  - Female
MH  - Fetal Development
MH  - Fetal Growth Retardation/*etiology/*metabolism/pathology
MH  - Kidney/*metabolism/pathology
MH  - Male
MH  - Maternal Exposure/*adverse effects
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Pregnancy
MH  - *Prenatal Exposure Delayed Effects
MH  - Proteomics/methods
MH  - Random Allocation
MH  - Smoking/*adverse effects
PMC - PMC3699329
MID - NIHMS378636
EDAT- 2012/05/19 06:00
MHDA- 2012/12/10 06:00
PMCR- 2013/09/28
CRDT- 2012/05/19 06:00
PHST- 2011/04/07 00:00 [received]
PHST- 2012/04/23 00:00 [revised]
PHST- 2012/04/25 00:00 [accepted]
PHST- 2012/05/19 06:00 [entrez]
PHST- 2012/05/19 06:00 [pubmed]
PHST- 2012/12/10 06:00 [medline]
PHST- 2013/09/28 00:00 [pmc-release]
AID - S0300-483X(12)00161-8 [pii]
AID - 10.1016/j.tox.2012.04.015 [doi]
PST - ppublish
SO  - Toxicology. 2012 Sep 28;299(2-3):80-9. doi: 10.1016/j.tox.2012.04.015. Epub 2012 
      May 15.