Increased expression of high mobility group box protein 1 and vascular endothelial growth factor in placenta previa

Xie,Han; Qiao,Ping; Lu,Yi; Li,Ying; Tang,Yuping; Huang,Yiying; Bao,Yirong; Ying,Hao

doi:10.3892/mmr.2017.7682

Increased expression of high mobility group box protein 1 and vascular endothelial growth factor in placenta previa

Authors:
- Han Xie
- Ping Qiao
- Yi Lu
- Ying Li
- Yuping Tang
- Yiying Huang
- Yirong Bao
- Hao Ying
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Affiliations: Department of Obstetrics, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 201204, P.R. China, Department of Pathology, Shanghai First Maternity and Infant Hospital, Tongji University School of Medicine, Shanghai 201204, P.R. China
Published online on: October 2, 2017 https://doi.org/10.3892/mmr.2017.7682
Pages: 9051-9059

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Abstract

Placenta previa is often associated with preterm delivery, reduced birth weight, a higher frequency of placental accreta and postpartum haemorrhage, and increased likelihood of blood transfusion. The present study aimed to examine the expression of high mobility group box protein 1 (HMGB1) in the placenta of women with or without placenta previa. The study group consisted of placental tissues obtained from women with or without placenta previa. The expression levels of HMGB1 and vascular endothelial growth factor (VEGF) were evaluated in the placental tissues using reverse transcription‑quantitative polymerase chain reaction, western blotting and immunohistochemistry. The mRNA expression levels of HMGB1 and VEGF were signiﬁcantly increased in the placenta previa group compared with in the normal group. In addition, the placenta previa group exhibited increased HMGB1 and VEGF staining in vascular endothelial cells and trophoblasts. There were no significant differences in the expression of HMGB1 or VEGF between groups with or without placenta accreta or postpartum haemorrhage. The present study hypothesised that the increased expression of HMGB1 in the placenta may be associated with the pathogenesis of placenta previa by regulating the expression of the proangiogenic factor VEGF.

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