PMID- 20160138
OWN - NLM
STAT- MEDLINE
DCOM- 20100409
LR  - 20100324
IS  - 1945-7170 (Electronic)
IS  - 0013-7227 (Linking)
VI  - 151
IP  - 4
DP  - 2010 Apr
TI  - Maternal leukemia inhibitory factor (LIF) promotes fetal neurogenesis via a 
      LIF-ACTH-LIF signaling relay pathway.
PG  - 1853-62
LID - 10.1210/en.2009-0985 [doi]
AB  - Leukemia inhibitory factor (LIF) promotes the proliferation of neuronal 
      progenitor cells in the cerebrum. However, it remains unclear how fetal LIF level 
      is regulated. Here we show evidence that maternal LIF signals drive fetal LIF 
      levels via the placenta, thereby promoting neurogenesis in the fetal brain in 
      rats. Chronological changes showed that LIF concentration in fetal sera (FS) and 
      fetal cerebrospinal fluid peaked at gestational day (GD) 15.5, after the peak of 
      maternal LIF at GD14.5. LIF injection into rat dams at GD15.5 increased the level 
      of ACTH in FS and subsequently increased LIF levels in FS and fetal cerebrospinal 
      fluid. The elevation of fetal LIF after LIF injection into dams was inhibited by 
      in utero injection of anti-ACTH antibody into fetuses. Cultured 
      syncytiotrophoblasts, which express the LIF receptor and glycoprotein 130, were 
      induced to secrete ACTH and up-regulate Pomc expression by the addition of LIF. 
      Nucleated red blood cells from fetuses at GD15.5, but not GD13.5 or GD17.5, 
      displayed LIF secretion in response to ACTH. Moreover, injection of LIF into dams 
      at GD13.5 or GD17.5 did not result in elevation of ACTH or LIF in fetuses. The 
      labeling index of 5-bromo-2'-deoxyuridine-positive cells in the ventricular zone 
      of the cerebral neocortex increased 24 h after injection of LIF into dams at 
      GD15.5 but not GD13.5 or GD17.5. These results suggest that in rats maternal LIF 
      induces ACTH from the placenta, which in turn induces fetal nucleated red blood 
      cells to secrete LIF that finally increases neurogenesis in fetuses around GD15.
FAU - Simamura, Eriko
AU  - Simamura E
AD  - Department of Molecular and Cell Structural Science, Kanazawa Medical University, 
      Uchinada, Ishikawa 920-0293, Japan.
FAU - Shimada, Hiroki
AU  - Shimada H
FAU - Higashi, Nobuaki
AU  - Higashi N
FAU - Uchishiba, Maimi
AU  - Uchishiba M
FAU - Otani, Hiroki
AU  - Otani H
FAU - Hatta, Toshihisa
AU  - Hatta T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100216
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Leukemia Inhibitory Factor)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, OSM-LIF)
RN  - 133483-10-0 (Cytokine Receptor gp130)
RN  - 66796-54-1 (Pro-Opiomelanocortin)
RN  - 9002-60-2 (Adrenocorticotropic Hormone)
SB  - IM
MH  - Adrenal Glands/metabolism
MH  - Adrenocorticotropic Hormone/genetics/*metabolism
MH  - Age Factors
MH  - Analysis of Variance
MH  - Animals
MH  - Cell Line
MH  - Cells, Cultured
MH  - Cytokine Receptor gp130/genetics/metabolism
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Erythrocytes/metabolism
MH  - Female
MH  - Hypothalamo-Hypophyseal System/metabolism
MH  - Immunohistochemistry
MH  - Leukemia Inhibitory Factor/genetics/*metabolism
MH  - Maternal-Fetal Exchange/*physiology
MH  - Neurogenesis/*physiology
MH  - Pituitary Gland/metabolism
MH  - Pituitary-Adrenal System/metabolism
MH  - Placenta/metabolism
MH  - Pregnancy
MH  - Pro-Opiomelanocortin/genetics/metabolism
MH  - RNA, Messenger/genetics/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Receptors, OSM-LIF/genetics/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/*physiology
MH  - Time Factors
MH  - Trophoblasts/metabolism
EDAT- 2010/02/18 06:00
MHDA- 2010/04/10 06:00
CRDT- 2010/02/18 06:00
PHST- 2010/02/18 06:00 [entrez]
PHST- 2010/02/18 06:00 [pubmed]
PHST- 2010/04/10 06:00 [medline]
AID - en.2009-0985 [pii]
AID - 10.1210/en.2009-0985 [doi]
PST - ppublish
SO  - Endocrinology. 2010 Apr;151(4):1853-62. doi: 10.1210/en.2009-0985. Epub 2010 Feb 
      16.