PMID- 28322267
OWN - NLM
STAT- MEDLINE
DCOM- 20181114
LR  - 20211204
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 7
DP  - 2017 Mar 21
TI  - Exposure of pregnant mice to triclosan impairs placental development and nutrient 
      transport.
PG  - 44803
LID - 10.1038/srep44803 [doi]
LID - 44803
AB  - Triclosan (TCS) is associated with spontaneous abortions and fetal growth 
      restriction. Here, we showed that when pregnant mice were treated with 8 mg/kg 
      TCS (8-TCS mice) on gestational days (GD) 6-18 fetal body weights were lower than 
      controls. Placental weights and volumes were reduced in 8-TCS mice. The placental 
      proliferative cells and expression of PCNA and Cyclin D3 on GD13 were remarkably 
      decreased in 8-TCS mice. The decreases in activities and expression of placental 
      System A amino acid or glucose transporters on GD14 and GD17 were observed in 
      8-TCS mice. Levels of serum thyroxine (T4) and triiodothyronine (T3) were lower 
      in 8-TCS mice than those in controls. Declines of placental Akt, mTOR and P70S6K 
      phosphorylation in 8-TCS mice were corrected by L-thyroxinein (T4). Treating 
      8-TCS mice with T4 rescued the placental cell proliferation and recovered the 
      activity and expression of amino acid and glucose transporters, which were 
      sensitive to mTOR inhibition by rapamycin. Furthermore, the replacement of T4 
      could rescue the decrease in fetal body weight, which was blocked by rapamycin. 
      These findings indicate that TCS-induced hypothyroxinemia in gestation mice 
      through reducing Akt-mTOR signaling may impair placental development and nutrient 
      transfer leading to decreases in fetal body weight.
FAU - Cao, Xinyuan
AU  - Cao X
AD  - State Key Lab of Reproductive Medicine, Nanjing Medical University, Nanjing, 
      211166, China.
FAU - Hua, Xu
AU  - Hua X
AD  - Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
FAU - Wang, Xiaoli
AU  - Wang X
AD  - Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
AD  - Department of Pharmacology, Nanjing Medical University, Nanjing, 211166, China.
FAU - Chen, Ling
AU  - Chen L
AD  - State Key Lab of Reproductive Medicine, Nanjing Medical University, Nanjing, 
      211166, China.
AD  - Department of Physiology, Nanjing Medical University, Nanjing, 211166, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20170321
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (Amino Acid Transport Systems)
RN  - 0 (Glucose Transport Proteins, Facilitative)
RN  - 0 (Hormones)
RN  - 4NM5039Y5X (Triclosan)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - EC 2.7.11.1 (Ribosomal Protein S6 Kinases, 70-kDa)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Amino Acid Transport Systems/genetics/metabolism
MH  - Animals
MH  - Biological Transport
MH  - Cell Proliferation
MH  - Female
MH  - Fetal Growth Retardation/etiology/metabolism/pathology
MH  - Gene Expression Regulation/drug effects
MH  - Glucose Transport Proteins, Facilitative/genetics/metabolism
MH  - Hormones/blood
MH  - Maternal Exposure/*adverse effects
MH  - Mice
MH  - Organ Size
MH  - Placenta/*drug effects/*metabolism/pathology
MH  - Placentation/*drug effects
MH  - Pregnancy
MH  - Proto-Oncogene Proteins c-akt/metabolism
MH  - Ribosomal Protein S6 Kinases, 70-kDa/metabolism
MH  - Signal Transduction/drug effects
MH  - TOR Serine-Threonine Kinases/metabolism
MH  - Triclosan/*adverse effects
PMC - PMC5359620
COIS- The authors declare no competing financial interests.
EDAT- 2017/03/23 06:00
MHDA- 2018/11/15 06:00
PMCR- 2017/03/21
CRDT- 2017/03/22 06:00
PHST- 2016/09/06 00:00 [received]
PHST- 2017/02/14 00:00 [accepted]
PHST- 2017/03/22 06:00 [entrez]
PHST- 2017/03/23 06:00 [pubmed]
PHST- 2018/11/15 06:00 [medline]
PHST- 2017/03/21 00:00 [pmc-release]
AID - srep44803 [pii]
AID - 10.1038/srep44803 [doi]
PST - epublish
SO  - Sci Rep. 2017 Mar 21;7:44803. doi: 10.1038/srep44803.