PMID- 34957095
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211228
IS  - 2296-634X (Print)
IS  - 2296-634X (Electronic)
IS  - 2296-634X (Linking)
VI  - 9
DP  - 2021
TI  - Upregulation of Fibrinogen-Like 1 Expression Contributes to Reducing the 
      Progression of Preeclampsia.
PG  - 757643
LID - 10.3389/fcell.2021.757643 [doi]
LID - 757643
AB  - Fibrinogen-like 1 (FGL1) is involved in liver injury and liver regeneration, but 
      its role in placenta and preeclampsia (PE) remains unclear. We assessed FGL1 
      expression in serum and placenta from L-NAME-induced PE-like mouse and in women 
      with (n = 38) and without (n = 42) PE. For the mouse study, pregnant C57Bl/6 
      mouse (n = 6/group) were subcutaneously administered L-NAME with or without FGL1 
      once daily starting on days 7-14 of pregnancy and were sacrificed on gestational 
      day (GD) 20. Maternal body weight, blood pressure, and urinary protein were 
      assessed during GDs 8-20. The weight and length of the placenta and fetus were 
      assessed. The placental structure was evaluated using hematoxylin staining. In 
      the human study, the sera of the pregnant women during the late trimester were 
      assessed with enzyme-linked immunosorbent assays (ELISAs). FGL1 expression in 
      human trophoblast cell lines under L-NAME stimulation was measured using Western 
      blotting and immunofluorescence staining. The detected FGL1 protein levels in 
      serum and placenta were both significantly upregulated in patients and mouse with 
      PE compared with those in the non-PE groups. FGL1 treatment decreased maternal 
      hypertension and proteinuria, decreased fetal weight in mouse with PE, 
      downregulated proinflammatory cytokine (interleukin-1b and interleukin-6) levels, 
      and maintained the balance between antiangiogenic (fms-like tyrosine kinase-1) 
      and proangiogenic (placental growth factor) substances in the placenta. 
      L-NAME-upregulated FGL1 expression was inhibited following overexpression of 
      FoxO3a. In summary, FoxO3a reduction is a potential pathophysiological mechanism 
      leading to upregulated placental FGL1 expression that may play a pivotal role in 
      preventing PE progression.
CI  - Copyright (c) 2021 Cheng, Chen, Wu, Lai, Lee, Lin, Shiau, Wu and Kang.
FAU - Cheng, Tsung-Lin
AU  - Cheng TL
AD  - Department of Physiology, School of Medicine, College of Medicine, Kaohsiung 
      Medical University, Kaohsiung, Taiwan.
AD  - Regenerative Medicine and Cell Therapy Research Center, Kaohsiung Medical 
      University, Kaohsiung, Taiwan.
FAU - Chen, Chung-Hwan
AU  - Chen CH
AD  - Regenerative Medicine and Cell Therapy Research Center, Kaohsiung Medical 
      University, Kaohsiung, Taiwan.
AD  - Orthopaedic Research Center, Kaohsiung Medical University, Kaohsiung, Taiwan.
AD  - Department of Orthopedics, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung 
      Medical University, Kaohsiung, Taiwan.
AD  - Division of Adult Reconstruction Surgery, Department of Orthopedics, Kaohsiung 
      Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan.
FAU - Wu, Meng-Hsing
AU  - Wu MH
AD  - Department of Obstetrics and Gynecology, National Cheng Kung University Hospital, 
      College of Medicine, National Cheng Kung University, Tainan, Taiwan.
FAU - Lai, Chao-Han
AU  - Lai CH
AD  - Department of Biochemistry and Molecular Biology, College of Medicine, National 
      Cheng Kung University, Tainan, Taiwan.
AD  - Department of Surgery, National Cheng Kung University Hospital, College of 
      Medicine, National Cheng Kung University, Tainan, Taiwan.
FAU - Lee, Ko-Hung
AU  - Lee KH
AD  - An-an Women and Children Clinic, Tainan, Taiwan.
FAU - Lin, Sheng-Hsiang
AU  - Lin SH
AD  - College of Medicine, Institute of Clinical Medicine, National Cheng Kung 
      University, Tainan, Taiwan.
FAU - Shiau, Ai-Li
AU  - Shiau AL
AD  - Department of Microbiology and Immunology, College of Medicine, National Cheng 
      Kung University, Tainan, Taiwan.
FAU - Wu, Chao-Liang
AU  - Wu CL
AD  - Department of Biochemistry and Molecular Biology, College of Medicine, National 
      Cheng Kung University, Tainan, Taiwan.
FAU - Kang, Lin
AU  - Kang L
AD  - Department of Obstetrics and Gynecology, National Cheng Kung University Hospital, 
      College of Medicine, National Cheng Kung University, Tainan, Taiwan.
LA  - eng
PT  - Journal Article
DEP - 20211208
PL  - Switzerland
TA  - Front Cell Dev Biol
JT  - Frontiers in cell and developmental biology
JID - 101630250
PMC - PMC8692364
OTO - NOTNLM
OT  - embryo (animal)
OT  - fibrinogen-like 1
OT  - placenta
OT  - preeclampsia
OT  - proinflammatory cytokines
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2021/12/28 06:00
MHDA- 2021/12/28 06:01
PMCR- 2021/01/01
CRDT- 2021/12/27 06:33
PHST- 2021/08/13 00:00 [received]
PHST- 2021/11/16 00:00 [accepted]
PHST- 2021/12/27 06:33 [entrez]
PHST- 2021/12/28 06:00 [pubmed]
PHST- 2021/12/28 06:01 [medline]
PHST- 2021/01/01 00:00 [pmc-release]
AID - 757643 [pii]
AID - 10.3389/fcell.2021.757643 [doi]
PST - epublish
SO  - Front Cell Dev Biol. 2021 Dec 8;9:757643. doi: 10.3389/fcell.2021.757643. 
      eCollection 2021.