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Updated: Feb 18, 2026

Trophoblast Cell Recovery from Angiogenesis-Tube Formation Assay for Differentiation Marker Expression Analysis
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Complement 5a-mediated trophoblasts dysfunction is involved in the development of pre-eclampsia.

Yu Ma1, Ling-Ran Kong1, Qian Ge1

  • 1State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Hypertension, Department of Hypertension, Ruijin Hospital and Shanghai Institute of Hypertension, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Journal of Cellular and Molecular Medicine
|November 24, 2017
PubMed
Summary

Complement 5a (C5a) and its receptor (C5aR) pathway in the placenta drives pre-eclampsia (PE) development by impairing trophoblast function. Targeting this pathway offers a potential new treatment for PE.

Keywords:
C5a receptorangiogenesisarterial stiffnesscomplement 5aplacentapre-eclampsiatrophoblasts

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Area of Science:

  • Obstetrics and Gynecology
  • Immunology
  • Pathology

Background:

  • Pre-eclampsia (PE) is a severe pregnancy complication with significant maternal and neonatal risks.
  • The complement system's role in PE pathogenesis is increasingly recognized, but detailed mechanisms remain unclear.

Purpose of the Study:

  • To elucidate the cellular and molecular mechanisms of complement activation in pre-eclampsia.
  • To investigate the role of complement 5a (C5a) and its receptor (C5aR) in placental development and PE.

Main Methods:

  • Immunohistochemical analysis of placental C5a deposition and C5aR expression in PE patients.
  • In vitro studies on trophoblast cells treated with C5a, including assessment of angiogenic factors (sFlt1, PIGF) and cell functions (migration, tube formation).
  • siRNA-mediated knockdown of C5aR in trophoblasts.
  • Measurement of maternal serum C5a levels and correlation with blood pressure and arterial stiffness.

Main Results:

  • Elevated C5a deposition and C5aR expression were observed in placentas from women with PE.
  • C5a induced an anti-angiogenic phenotype in trophoblasts by altering sFlt1 and PIGF levels.
  • C5a inhibited trophoblast migration and tube formation; C5aR knockdown reversed these effects.
  • Increased maternal serum C5a levels in PE correlated positively with blood pressure and arterial stiffness.

Conclusions:

  • The placental C5a/C5aR pathway is a key contributor to PE pathogenesis by inducing trophoblast dysfunction.
  • C5a/C5aR signaling disrupts normal placental development and angiogenic balance.
  • C5a represents a potential therapeutic target for pre-eclampsia.