High-Mobility Group Box 1 From Hypoxic Trophoblasts Promotes Endothelial Microparticle Production and Thrombophilia in Preeclampsia

Hu, Yae; Yan, Rui; Zhang, Ce; Zhou, Zhichao; Li, Meng; Wang, Can; Zhang, Hong; Dong, Liang; Zhou, Tiantian; Dong, Ningzheng; Wu, Qingyu

doi:10.1161/atvbaha.118.310940

Cited by 37 publications

(34 citation statements)

References 55 publications

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“…As a late inflammatory factor, HMGB1 is considered to be closely related to a variety of inflammatory diseases [ 7 , 8 ]. Recently, HMGB1 was found to be highly expressed in the placenta of PE women [ 9 , 10 ]. Placental hypoxia can promote the expression and release of HMGB1 from trophoblasts [ 9 ].…”

Section: Discussionmentioning

confidence: 99%

“…After damage of pathogenic factors, HMGB1 interacts with receptor for advanced glycation end-products and Toll-like receptors through active and passive release, causing the release of inflammatory mediators and stimulating the immune inflammatory response of the body [ 7 , 8 ]. It had been reported that placental hypoxia induced the expression and release of HMGB1 from trophoblasts [ 9 ]. Accumulating reports presented high levels of placental HMGB1 in women with PE [ 9 , 10 ].…”

Section: Introductionmentioning

confidence: 99%

“…It had been reported that placental hypoxia induced the expression and release of HMGB1 from trophoblasts [ 9 ]. Accumulating reports presented high levels of placental HMGB1 in women with PE [ 9 , 10 ]. Moreover, increasing evidence suggests that placental hypoxia-induced HMGB1 release plays a central role in endothelial dysfunction [ 9 , 11 ].…”

Section: Introductionmentioning

confidence: 99%

“…Accumulating reports presented high levels of placental HMGB1 in women with PE [ 9 , 10 ]. Moreover, increasing evidence suggests that placental hypoxia-induced HMGB1 release plays a central role in endothelial dysfunction [ 9 , 11 ]. Therefore, HMGB1 may be an important therapy target for PE.…”

Section: Introductionmentioning

confidence: 99%

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Epigallocatechin Gallate (EGCG) Improves Anti-Angiogenic State, Cell Viability, and Hypoxia-Induced Endothelial Dysfunction by Downregulating High Mobility Group Box 1 (HMGB1) in Preeclampsia

et al. 2020

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Background Preeclampsia (PE) is a serious complication of pregnancy with no effective therapy. This study assessed whether epigallocatechin gallate (EGCG) could reduce the production of anti-angiogenic factors, improve cell viability, and suppress endothelial dysfunction in vitro via regulating high mobility group box 1 (HMGB1) in preeclampsia. Material/Methods Human umbilical vein endothelial cells (HUVECs) grown in conditioned medium from hypoxic JEG-3 cells were used to investigate the effects of EGCG on anti-angiogenic state, cell viability, and markers of endothelial dysfunction. To confirm that EGCG exerted its effects via HMGB1, we also examined the impact of EGCG on anti-angiogenic state, cell viability, and endothelial dysfunction following HMGB1 treatment in vitro . Results EGCG inhibited HMGB1 expression in hypoxic trophoblast cells in a dose-dependent manner. In addition, EGCG relieved anti-angiogenic state and endothelial dysfunction in hypoxic trophoblast cells by downregulating HMGB1. Moreover, EGCG dose-dependently promoted cell proliferation by downregulating HMGB1. Conclusions Taken together, our data show the protective role of EGCG in preeclampsia and revealed EGCG-mediated effects on the production of anti-angiogenic factors, cell viability, and endothelial dysfunction through downregulating HMGB1. These observations suggest that EGCG is a novel therapeutic candidate for preeclampsia.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Epigallocatechin Gallate (EGCG) Improves Anti-Angiogenic State, Cell Viability, and Hypoxia-Induced Endothelial Dysfunction by Downregulating High Mobility Group Box 1 (HMGB1) in Preeclampsia

et al. 2020

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“…For the identication of water inrush in the coal mine, the traditional methods are mostly based on hydrochemistry, 9 through which we obtain pH, ion concentration, conductivity and other parameters to establish the classication model of mine water inrush. 10 However, hydrochemical methods have some limitations such as being time-consuming 11 and requiring specialized instruments and skilled operators, which restrict their applications in online warning of mine water inrush. To overcome these shortcomings, great focus has been put on developing fast, online and reliable methods for the identication of mine water inrush.…”

Section: Introductionsmentioning

confidence: 99%

Identification of mine water inrush using laser-induced fluorescence spectroscopy combined with one-dimensional convolutional neural network

Zhou

Yan

et al. 2019

RSC Adv.

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Ectopic expression of human airway trypsin‐like protease 4 in acute myeloid leukemia promotes cancer cell invasion and tumor growth

Yan

et al. 2019

Cancer Medicine

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Transmembrane serine proteases have been implicated in the development and progression of solid and hematological cancers. Human airway trypsin‐like protease 4 (HAT‐L4) is a transmembrane serine protease expressed in epithelial cells and exocrine glands. In the skin, HAT‐L4 is important for normal epidermal barrier function. Here, we report an unexpected finding of ectopic HAT‐L4 expression in neutrophils and monocytes from acute myeloid leukemia (AML) patients. Such expression was not detected in bone marrow cells from normal individuals or patients with chronic myeloid leukemia, acute lymphocytic leukemia and chronic lymphocytic leukemia. In AML patients who underwent chemotherapy, persistent HAT‐L4 expression in bone marrow cells was associated with minimal residual disease and poor prognostic outcomes. In culture, silencing HAT‐L4 expression in AML–derived THP‐1 cells by short hairpin RNAs inhibited matrix metalloproteinase‐2 activation and Matrigel invasion. In mouse xenograft models, inhibition of HAT‐L4 expression reduced the proliferation and growth of THP‐1 cell–derived tumors. Our results indicate that ectopic HAT‐L4 expression is a pathological mechanism in AML and that HAT‐L4 may be used as a cell surface marker for AML blast detection and targeting.

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High-Mobility Group Box 1 From Hypoxic Trophoblasts Promotes Endothelial Microparticle Production and Thrombophilia in Preeclampsia

Abstract: Our results indicate that placental hypoxia-induced HMGB1 expression and release from trophoblasts are important mechanism underlying increased circulating endothelial microparticles and thrombophilia in preeclampsia.

Cited by 37 publications

References 55 publications

Epigallocatechin Gallate (EGCG) Improves Anti-Angiogenic State, Cell Viability, and Hypoxia-Induced Endothelial Dysfunction by Downregulating High Mobility Group Box 1 (HMGB1) in Preeclampsia

Epigallocatechin Gallate (EGCG) Improves Anti-Angiogenic State, Cell Viability, and Hypoxia-Induced Endothelial Dysfunction by Downregulating High Mobility Group Box 1 (HMGB1) in Preeclampsia

Identification of mine water inrush using laser-induced fluorescence spectroscopy combined with one-dimensional convolutional neural network

Ectopic expression of human airway trypsin‐like protease 4 in acute myeloid leukemia promotes cancer cell invasion and tumor growth

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