PMID- 26065916
OWN - NLM
STAT- MEDLINE
DCOM- 20160606
LR  - 20220318
IS  - 2045-2322 (Electronic)
IS  - 2045-2322 (Linking)
VI  - 5
DP  - 2015 Jun 12
TI  - Vitamin D3 inhibits lipopolysaccharide-induced placental inflammation through 
      reinforcing interaction between vitamin D receptor and nuclear factor kappa B p65 
      subunit.
PG  - 10871
LID - 10.1038/srep10871 [doi]
LID - 10871
AB  - It is increasingly recognized that vitamin D3 (VitD3) has an anti-inflammatory 
      activity. The present study investigated the effects of maternal VitD3 
      supplementation during pregnancy on LPS-induced placental inflammation and fetal 
      intrauterine growth restriction (IUGR). All pregnant mice except controls were 
      intraperitoneally injected with LPS (100 mug/kg) daily from gestational day 
      (GD)15-17. In VitD3 + LPS group, pregnant mice were orally administered with 
      VitD3 (25 mug/kg) before LPS injection. As expected, maternal LPS exposure caused 
      placental inflammation and fetal IUGR. Interestingly, pretreatment with VitD3 
      repressed placental inflammation and protected against LPS-induced fetal IUGR. 
      Further analysis showed that pretreatment with VitD3, which activated placental 
      vitamin D receptor (VDR) signaling, specifically suppressed LPS-induced 
      activation of nuclear factor kappa B (NF-kappaB) and significantly blocked nuclear 
      translocation of NF-kappaB p65 subunit in trophoblast gaint cells of the labyrinth 
      layer. Conversely, LPS, which activated placental NF-kappaB signaling, suppressed 
      placental VDR activation and its target gene expression. Moreover, VitD3 
      reinforced physical interaction between placental VDR and NF-kappaB p65 subunit. The 
      further study demonstrates that VitD3 inhibits placental NF-kappaB signaling in 
      VDR-dependent manner. These results provide a mechanistic explanation for 
      VitD3-mediated anti-inflammatory activity. Overall, the present study provides 
      evidence for roles of VDR as a key regulator of placental inflammation.
FAU - Chen, Yuan-Hua
AU  - Chen YH
AD  - 1] School of Public Health, Anhui Medical University, Hefei, China [2] Anhui 
      Provincial Key Laboratory of Population Health &Aristogenics, Anhui Medical 
      University, Hefei, China [3] School of Basic Medical Science, Anhui Medical 
      University, Hefei, 230032, China.
FAU - Yu, Zhen
AU  - Yu Z
AD  - 1] School of Public Health, Anhui Medical University, Hefei, China [2] Anhui 
      Provincial Key Laboratory of Population Health &Aristogenics, Anhui Medical 
      University, Hefei, China.
FAU - Fu, Lin
AU  - Fu L
AD  - School of Public Health, Anhui Medical University, Hefei, China.
FAU - Wang, Hua
AU  - Wang H
AD  - 1] School of Public Health, Anhui Medical University, Hefei, China [2] Anhui 
      Provincial Key Laboratory of Population Health &Aristogenics, Anhui Medical 
      University, Hefei, China.
FAU - Chen, Xue
AU  - Chen X
AD  - School of Public Health, Anhui Medical University, Hefei, China.
FAU - Zhang, Cheng
AU  - Zhang C
AD  - 1] School of Public Health, Anhui Medical University, Hefei, China [2] Anhui 
      Provincial Key Laboratory of Population Health &Aristogenics, Anhui Medical 
      University, Hefei, China.
FAU - Lv, Zheng-Mei
AU  - Lv ZM
AD  - School of Basic Medical Science, Anhui Medical University, Hefei, 230032, China.
FAU - Xu, De-Xiang
AU  - Xu DX
AD  - 1] School of Public Health, Anhui Medical University, Hefei, China [2] Anhui 
      Provincial Key Laboratory of Population Health &Aristogenics, Anhui Medical 
      University, Hefei, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150612
PL  - England
TA  - Sci Rep
JT  - Scientific reports
JID - 101563288
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Receptors, Calcitriol)
RN  - 0 (Rela protein, mouse)
RN  - 0 (Transcription Factor RelA)
RN  - 1C6V77QF41 (Cholecalciferol)
SB  - IM
MH  - Animals
MH  - Cholecalciferol/*pharmacology
MH  - Female
MH  - *Fetal Growth Retardation/chemically induced/drug therapy/metabolism/pathology
MH  - Inflammation/chemically induced/drug therapy/metabolism/pathology
MH  - Lipopolysaccharides/*toxicity
MH  - Male
MH  - Mice
MH  - Mice, Inbred ICR
MH  - *Placenta/metabolism/pathology
MH  - *Placenta Diseases/chemically induced/drug therapy/metabolism/pathology
MH  - Pregnancy
MH  - Receptors, Calcitriol/*metabolism
MH  - Signal Transduction/*drug effects
MH  - Transcription Factor RelA/*metabolism
PMC - PMC4464284
EDAT- 2015/06/13 06:00
MHDA- 2016/06/09 06:00
PMCR- 2015/06/12
CRDT- 2015/06/13 06:00
PHST- 2015/01/21 00:00 [received]
PHST- 2015/05/01 00:00 [accepted]
PHST- 2015/06/13 06:00 [entrez]
PHST- 2015/06/13 06:00 [pubmed]
PHST- 2016/06/09 06:00 [medline]
PHST- 2015/06/12 00:00 [pmc-release]
AID - srep10871 [pii]
AID - 10.1038/srep10871 [doi]
PST - epublish
SO  - Sci Rep. 2015 Jun 12;5:10871. doi: 10.1038/srep10871.