Mitochondrial dysfunction-induced high hCG associated with development of fetal growth restriction and pre-eclampsia with fetal growth restriction

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  • Kiyokoba, Ryo
    Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University Department of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University
  • Uchiumi, Takeshi
    Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University Department of Health Sciences, Graduate School of Medical Sciences, Kyushu University
  • Yagi, Mikako
    Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University Department of Health Sciences, Graduate School of Medical Sciences, Kyushu University
  • Toshima, Takahiro
    Department of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University
  • Tsukahara, Shigehiro
    Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University
  • Fujita, Yasuyuki
    Department of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University
  • Kato, Kiyoko
    Department of Obstetrics and Gynecology, Graduate School of Medical Sciences, Kyushu University
  • Kang, Dongchon
    Department of Clinical Chemistry and Laboratory Medicine, Graduate School of Medical Sciences, Kyushu University

Description

Fetal growth restriction (FGR) and pre-eclampsia with fetal growth restriction (PE/FGR) are high-risk perinatal diseases that may involve high levels of human chorionic gonadotropin (hCG) and mitochondrial dysfunction. However, little is known about how these factors affect placental function. We investigated how mitochondrial dysfunction and high hCG expression affected placental function in unexplained FGR and PE/FGR. We observed elevated expression of hCGβ and growth differentiation factor 15 mRNA and protein levels in the placenta with both diseases. Likewise, antiangiogenic factors, such as Ang2, IP10, sFlt1, IL8, IL1B, and TNFα, were also upregulated at the mRNA level. In addition, the expression of COXI and COXII which encoded by mitochondrial DNA were significantly decreased in both diseases, suggesting that mitochondrial translation was impaired. Treatment with hCG increased Ang2, IP10, IL8, and TNFα mRNA levels in a dose-dependent manner via the p38 and JNK pathways. Mitochondrial translation inhibitors increased hCGβ expression through stabilization of HIF1α, and increased IL8 and TNFα mRNA expression. These results revealed that high expression of hCG due to mitochondrial translational dysfunction plays an important role in the pathogenesis of FGR and PE/FGR.

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