The depletion of MARVELD1 leads to murine placenta accreta via integrin β4‐dependent trophoblast cell invasion

Chen, Yue; Zhang, Hui; Han, Fangfang; Yue, Lei; Qiao, Chunxiao; Zhang, Yao; Dou, Peng; Liu, Weizhe; Yu, Li

doi:10.1002/jcp.26098

Cited by 19 publications

(14 citation statements)

References 38 publications

(39 reference statements)

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“…Chen et al investigated the role of MARVELD1, a nuclear protein that inhibits cell migration in mice [ 41 , 42 ]. Knockout of placental MARVELD1 in a transgenic mouse model induced the downregulation of integrin β 4 which resulted in increased trophoblast cell invasion.…”

Section: Molecular Biologymentioning

confidence: 99%

Placenta Accreta Spectrum: A Review of Pathology, Molecular Biology, and Biomarkers

et al. 2018

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Background. Placenta accreta spectrum (PAS) is a condition of abnormal placental invasion encompassing placenta accreta, increta, and percreta and is a major cause of severe maternal morbidity and mortality. The diagnosis of a PAS is made on the basis of histopathologic examination and characterised by an absence of decidua and chorionic villi are seen to directly adjacent to myometrial fibres. The underlying molecular biology of PAS is a complex process that requires further research; for ease, we have divided these processes into angiogenesis, proliferation, and inflammation/invasion. A number of diagnostic serum biomarkers have been investigated in PAS, including human chorionic gonadotropin (HCG), pregnancy-associated plasma protein-A (PAPP-A), and alpha-fetoprotein (AFP). They have shown variable reliability and variability of measurement depending on gestational age at sampling. At present, a sensitive serum biomarker for invasive placentation remains elusive. In summary, there are a limited number of studies that have contributed to our understanding of the molecular biology of PAS, and additional biomarkers are needed to aid diagnosis and disease stratification.

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Section: Molecular Biologymentioning

confidence: 99%

Placenta Accreta Spectrum: A Review of Pathology, Molecular Biology, and Biomarkers

et al. 2018

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“…Our previous studies had illustrated that MARVELD1 was downexpression in non–small cell lung cancer and hepatocellular carcinoma, and could regulate cell proliferation and cell migration . To thoroughly investigate the alterations of MARVELD1 expression and characteristics, MARVELD1 gene expression profiling in 26 cancer cells was performed by CCLPA cDNA hybridization which was treated with 25 stress factors (Figure A).…”

Section: Resultsmentioning

confidence: 99%

MARVELD1 interacting with catalase regulates reactive oxygen species metabolism and mediates the sensitivity to chemotherapeutic drugs in epithelial tumors of the reproductive system

Zhang

Han

Shi

et al. 2019

Molecular Carcinogenesis

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Previous investigations have found that MARVEL domain-containing 1 (MARVELD1) could inhibit tumor cell proliferation and enhance the sensitivity to chemotherapeutic drugs in hepatocellular carcinoma. Hence, it may be a valuable therapeutic target. In the study, we analyzed the responsive changes of MARVELD1 to 25 stress factors and expression of MARVELD1 in epithelial tumors of the reproductive system. We found that MARVELD1 was transferred to the cytoplasm and mitochondria under cell stress. And under cellular stress, the reactive oxygen species (ROS) levels decreased in MARVELD1 expressed cells while increased in the cells of MARVELD1-specific siRNA treatment. Meanwhile, MARVELD1 overexpression significantly promoted the inhibition of tumor cell proliferation under cellular stress via affecting ROS metabolism, not cell cycle. In xenograft tumor tissues with MARVELD1 expression, the tumor growth was inhibited and accompanied by the lower ROS levels. Furthermore, we identified that MARVELD1 could interact with catalase (CAT) to enhance latter activity and maintain stability. And the enhanced sensitivity to chemotherapeutic drugs clearly depended on the ability of MARVELD1 scavenge the ROS in carcinoma cells of the reproductive system. Our findings clearly explain that MARVELD1 may regulate tumor cell proliferation and sensitivity to chemotherapeutic drugs via reducing the exorbitant ROS. The mechanism was that MARVELD1 interacted with CAT to maintain latter stability, and then ensure continuous ROS scavenge.

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“…Thus, in the presence of factors secreted in physiologically forming placenta, the trophoblast raises the expression of receptors to TNFa, lymphotoxin, MCP-1, RANTES, MIP-1a, Leptin, and EGF (Figure 3 and Table 1). The parallel decrease of CD104 expression, the extracellular matrix component receptor (Table 1), along with E-cadherin reduced expression may increase the trophoblast invasiveness [6]. However, HGFR, CD49f, CD54, and HLA-G expression remains quite high and does not change in the presence of placenta secreted factors neither in normal nor in pathology case (Figure 3).…”

Section: Discussionmentioning

confidence: 96%

Receptor expression by JEG-3 trophoblast cells in the presence of placenta secreted factors

Bazhenov

Furaeva

Степанова

et al. 2019

Gynecological Endocrinology

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Preeclampsia still remains one of the most severe pregnancy complications and is an actual problem in the obstetrics practice. At present, the joint impact of cytokines and other placenta secreted factors on trophoblast cell functional activity during preeclampsia complicated pregnancy remains unclear. The aim of the study is to estimate the surface receptors expression by trophoblast cells in the presence of placenta secreted factors during physiological pregnancy and at preeclampsia. Trophoblast cells of the JEG-3 line were incubated in the presence of supernatants obtained by cultivation of placentas from women with physiological pregnancy and with preeclampsia. Surface receptors expression by trophoblast cells was estimated by FACS Canto II flow cytometer. It was established that in the third trimester both under normal and pathological conditions, the placenta secreted factors impact on the cytokine receptor expression by trophoblast differs while the trophoblast response capacity to the migration and proliferation stimulating and inhibiting signals remains stable. JEG-3 line cells enhanced the expression of CD186, CD140a, Integrin b6, VE-cadherin, CD29, and CD140a in the case of incubation in the presence of placenta supernatants from the third-trimester pregnancy complicated with preeclampsia compared to incubation in the presence of placenta supernatants form the third trimester of physiological pregnancy.

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The depletion of MARVELD1 leads to murine placenta accreta via integrin β4‐dependent trophoblast cell invasion

Cited by 19 publications

References 38 publications

Placenta Accreta Spectrum: A Review of Pathology, Molecular Biology, and Biomarkers

Placenta Accreta Spectrum: A Review of Pathology, Molecular Biology, and Biomarkers

MARVELD1 interacting with catalase regulates reactive oxygen species metabolism and mediates the sensitivity to chemotherapeutic drugs in epithelial tumors of the reproductive system

Receptor expression by JEG-3 trophoblast cells in the presence of placenta secreted factors

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