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Role of Placenta fibrinogen-like 1 (FGL1) in the Pre-Eclampsia progression: a functional study
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  • Tsung-Lin Cheng,
  • Chung-Hwan Chen,
  • Meng-Hsing Wu,
  • Chao-Han Lai,
  • Ko-Hung Lee,
  • Sheng-Hsiang Lin,
  • Ai-Li Shiau,
  • Chao-Liang Wu,
  • Kang Lin
Tsung-Lin Cheng

Corresponding Author:[email protected]

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Chung-Hwan Chen
Kaohsiung Medical University
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Meng-Hsing Wu
National Cheng Kung University Hospital
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Chao-Han Lai
National Cheng Kung University Hospital
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Ko-Hung Lee
An-an Women and Children Clinic
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Sheng-Hsiang Lin
National Cheng Kung University College of Medicine
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Ai-Li Shiau
National Cheng Kung University College of Medicine
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Chao-Liang Wu
National Cheng Kung University College of Medicine
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Kang Lin
National Cheng Kung University Hospital
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Abstract

Objective: To study the role of placenta fibrinogen-like 1 (FGL1) during pre-eclampsia (PE) progression. Design: A case-control study combined with the experimental research of the cellular and PE mouse model. Setting: FGL1 is a protein involved in liver regeneration, but its role in the placenta and PE remains uninvestigated. Population or Sample: Serum and placenta from the PE mouse model and in women with (n = 38) and without (n = 42) PE were analyzed. Methods: Pregnant C57Bl/6 mice (n = 6) were administered L-NAME subcutaneously with or without FGL1 once daily starting on day 7–14 of pregnancy until sacrifice. Maternal body weight, blood pressure, urinary protein, weight and length of the placenta and fetus were assessed. The placental structure was evaluated using histochemistry staining. The sera of pregnant women during the late trimester were quantified with ELISA. Main Outcome Measures: FGL1 expression in serum and placenta during PE, and treatment outcome of FGL1. Results: FGL1 expression in both serum and placenta was significantly upregulated in patients with PE and mice compared with control groups. FGL1 treatment decreased maternal hypertension, and proteinuria, ameliorated fetal weight in PE mice, downregulated proinflammatory cytokines (interleukin-1b and -6), and maintained the balance between antiangiogenic (sFlt-1, soluble fms-like tyrosine kinase-1) and proangiogenic substances (Pgf, placental growth factor) in the placenta. Conclusions: Placental FGL1 upregulation plays a pivotal role in reducing PE progression. Funding: Ministry of Science and Technology (MOST 106-2314-B-006-066, 108-2314-B-006-062), Taiwan; National Cheng Kung University Hospital (NCKUH-10604002, NCKUH-10705015, NCKUH-10902008); Kaohsiung Medical University (KMU-TC108A02, KMUH-DK(A)110003)