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The Globular Heads of the C 1q Receptor Regulate Apoptosis in Human Extravillous Cytotrophoblast‐derived Transformed Cells via a Mitochondria‐dependent Pathway
Author(s) -
Wang Ying,
Guo Shuyu,
Gu Pingqing,
Wang Xiaoman,
Sun Ning,
Gao Lingjuan
Publication year - 2014
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12160
Subject(s) - microbiology and biotechnology , apoptosis , cytotrophoblast , mitochondrion , chemistry , receptor , biology , biochemistry , genetics , fetus , placenta , pregnancy
Problem The receptor for the globular head of human C1q ( gC 1qR) predominantly localizes to the mitochondrial matrix. gC 1qR 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 gC 1qR 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 gC 1qR 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 Ca 2+ and changes in the mitochondrial membrane potential (Δψm). Results The expression of the gC 1qR gene was significantly increased in spontaneous abortion samples relative to induced abortion samples. HTR‐8/SVneo and HPT‐8 cells transfected with a gC 1qR 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 gC 1qR induces apoptosis through mitochondria‐dependent pathways in human EVCT‐derived transformed cells.