Get access

The Globular Heads of the C1q Receptor Regulate Apoptosis in Human Extravillous Cytotrophoblast-derived Transformed Cells via a Mitochondria-dependent Pathway

Authors

  • Ying Wang,

    1. Clinical Laboratory, Harbin Medical University Cancer Hospital, Harbin, China
    Search for more papers by this author
  • Shu-yu Guo,

    1. National Centre for Epidemiology and Population Health, The Australian National University, Canberra, Australia
    Search for more papers by this author
  • Ping-qing Gu,

    1. Department of Clinical Laboratory, State Key Laboratory of Reproductive Medicine, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing, China
    Search for more papers by this author
  • Xiao-man Wang,

    1. Department of Clinical Laboratory, State Key Laboratory of Reproductive Medicine, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing, China
    Search for more papers by this author
  • Ning Sun,

    1. Department of Clinical Laboratory, State Key Laboratory of Reproductive Medicine, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing, China
    Search for more papers by this author
  • Ling-juan Gao

    Corresponding author
    1. Department of Clinical Laboratory, State Key Laboratory of Reproductive Medicine, Nanjing Maternity and Child Health Care Hospital Affiliated to Nanjing Medical University, Nanjing, China
    • Correspondence

      Ling-juan Gao, Clinical Laboratory, Nanjing Maternity and Child Health Care Hospital, Tianfei Alley, Nanjing Mochou Road, 210004 Nanjing, China.

      E-mail: gaolingjuan@njmu.edu.cn

    Search for more papers by this author

Abstract

Problem

The receptor for the globular head of human C1q (gC1qR) predominantly localizes to the mitochondrial matrix. gC1qR mediates many biological responses, including growth perturbations, morphological abnormalities and the initiation of apoptosis. The purpose of this study was to investigate the relationship between gC1qR expression, mitochondrial dysfunction and the regulation of apoptosis in human extravillous cytotrophoblast (EVCT)-derived transformed cell lines (HTR-8/SVneo and HPT-8).

Method of study

gC1qR expression was examined in human placental villi using real-time qPCR and Western blot analysis. The apoptotic death of HTR-8/SVneo and HPT-8 cells was assessed using flow cytometric analysis. Mitochondrial function was assessed via ROS generation, the amount of cytosolic Ca2+ and changes in the mitochondrial membrane potential (Δψm).

Results

The expression of the gC1qR gene was significantly increased in spontaneous abortion samples relative to induced abortion samples. HTR-8/SVneo and HPT-8 cells transfected with a gC1qR vector showed upregulation of cellular apoptosis and mitochondrial dysfunction, interestingly, which were abrogated by the addition of metformin. Metformin may protect mitochondrial function.

Conclusion

These data support a mechanism whereby gC1qR induces apoptosis through mitochondria-dependent pathways in human EVCT-derived transformed cells.

Get access to the full text of this article

Ancillary