Fibrinogen-Like Protein 2-Associated Transcriptional and Histopathological Features of Immunological Preeclampsia

Robineau-Charette, Pascale; Grynspan, David; Benton, Samantha J.; Gaudet, Jeremiah; Cox, Brian; Vanderhyden, Barbara C.; Bainbridge, Shannon

doi:10.1161/hypertensionaha.120.14807

Cited by 7 publications

(4 citation statements)

References 33 publications

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“…TNF-α, CCL2, IFN-γ; Figure 3 ). Previously, descriptions of immune cell infiltration into the placental exchange region, and up-regulated placenta expression of similar pro-inflammatory mediators have been described in rodent models of LPS treatment in pregnancy ( 65 , 66 ) - findings that closely mimic observations made in human placentas from cases of inflammatory PE ( 1 , 6 , 67 ). Even though both Poly I:C and LPS are TLR activators, Poly I:C treatment, not LPS, in pregnant mice has been shown to modulate the expression of ATP-binding cassette (ABC) transporters in the JZ leading to cell death in that region ( 68 – 70 ).…”

Section: Discussionsupporting

confidence: 55%

A comparison of rat models that best mimic immune-driven preeclampsia in humans

Jahan,

Vasam,

Cariaco

et al. 2023

Front. Endocrinol.

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Preeclampsia (PE), a hypertensive pregnancy disorder, can originate from varied etiology. Placenta malperfusion has long been considered the primary cause of PE. However, we and others have showed that this disorder can also result from heightened inflammation at the maternal-fetal interface. To advance our understanding of this understudied PE subtype, it is important to establish validated rodent models to study the pathophysiology and test therapies. We evaluated three previously described approaches to induce inflammation-mediated PE-like features in pregnant rats: 1) Tumor necrosis factor-α (TNF-α) infusion via osmotic pump from gestational day (GD) 14-19 at 50ng/day/animal; 2) Polyinosinic:polycytidylic acid (Poly I:C) intraperitoneal (IP) injections from GD 10-18 (alternate days) at 10mg/kg/day/animal; and, 3) Lipopolysaccharide (LPS) IP injections from GD 13-18 at 20ug-70ug/kg/day per animal. Maternal blood pressure was measured by tail-cuff. Upon sacrifice, fetal and placenta weights were recorded. Placenta histomorphology was assessed using H&E sections. Placenta inflammation was determined by quantifying TNF-α levels and inflammatory gene expression. Placenta metabolic and mitochondrial health were determined by measuring mitochondrial respiration rates and placenta NAD+/NADH content. Of the three rodent models tested, we found that Poly I:C and LPS decreased both fetal weight and survival; and correlated with a reduction in region specific placenta growth. As the least effective model characterized, TNF-α treatment resulted in a subtle decrease in fetal/placenta weight and placenta mitochondrial respiration. Only the LPS model was able to induce maternal hypertension and exhibited pronounced placenta metabolic and mitochondrial dysfunction, common features of PE. Thus, the rat LPS model was most effective for recapitulating features observed in cases of human inflammatory PE. Future mechanistic and/or therapeutic intervention studies focuses on this distinct PE patient population may benefit from the employment of this rodent model of PE.

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Section: Discussionsupporting

confidence: 55%

A comparison of rat models that best mimic immune-driven preeclampsia in humans

Jahan,

Vasam,

Cariaco

et al. 2023

Front. Endocrinol.

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“…Among these 16 differential proteins, many proteins have been proved to be closely related to the development of endothelial vascular injury diseases (even preeclampsia). For example, angiotensin disorders can cause cardiovascular disease by raising blood pressure; elevated fibrinogen can aggravate the inflammatory response in pregnant women; placental growth factor can promote placental angiogenesis and has a nourishing effect on the growth of placental cells [24][25][26]. This provides a more comprehensive reference for us to study the mechanism of preeclampsia at the molecular level and also provides data support for the screening of relevant markers for early diagnosis of preeclampsia.…”

Section: Changes In Fetalmentioning

confidence: 95%

Analysis of Proteomic Characteristics of Peripheral Blood in Preeclampsia and Study of Changes in Fetal Arterial Doppler Parameters Based on Magnetic Nanoparticles

Zhou

Liu

Zhang

et al. 2021

Computational and Mathematical Methods in Medicine

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Background. Traditional mass spectrometry detection methods have low detection efficiency for low-abundance proteins, thus limiting the application of proteomic analysis in the diagnosis of preeclampsia. Magnetic nanomaterials have good superparamagnetism and have obvious advantages in the field of biological separation and enrichment. Aim. The objective of this study is to explore the value of superparamagnetic iron oxide nanoparticles in the proteomic analysis of preeclampsia. Materials and Methods. 42 patients and 40 normal pregnant women were selected in this study for analysis. Gene Ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis were performed to evaluate the function of these differential proteins. Proteomic analysis was used to analyze the differential proteins. Color Doppler ultrasound technology was used to detect changes in the blood flow of the fetal umbilical artery and cerebral artery. Results. 16 differential proteins in the serum of pregnant women with preeclampsia and normal pregnant women were detected. The 16 proteins are mainly related to angiogenesis and endothelial function proteins, coagulation cascade proteins, placental growth factor, and so on. Biological function analysis revealed that these proteins are mainly enriched in the nuclear factor kB (NF-κB) signaling pathway. Moreover, our data suggested that compared with the fetus in the uterus of normal pregnant women, the umbilical artery S/D, PI, and RI of the fetus in preeclampsia were greatly increased, and the cerebral artery S/D, PI, and RI were greatly decreased. Conclusion. Biological function analysis revealed that 16 proteins are mainly enriched in the NF-κB signaling pathway. Compared with the normal group, the umbilical artery S/D, PI, and RI of the preeclampsia group were greatly increased, and the cerebral artery S/D, PI, and RI were all greatly reduced. Our findings provided a more comprehensive reference for us to study the mechanism of preeclampsia at the molecular level and also provide data support for the screening of relevant markers for early diagnosis of preeclampsia.

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“…Preeclampsia (PE) is a complex disorder that affects 3%–8% of pregnant women(Robineau‐Charette et al, 2020). Severe PE progresses to acute pulmonary edema, refractory hypertension, and acute kidney injury (Sircar et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA PVT1 accelerates the growth of placental trophoblasts in preeclampsia through the microRNA‐24‐3p/HSD11B2 axis

Wei

Yuan

Yang

2022

Molecular Reproduction Devel

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Long noncoding RNA plasmacytoma variant translocation 1 (PVT1) is essential for the maintenance of normal functions of trophoblasts in preeclampsia (PE). This study aims to decipher the concrete mechanism of PVT1 with the microRNA-24-3p/Type-2 11βhydroxysteroid dehydrogenase (miR-24-3p/HSD11B2) axis in PE. PVT1, miR-24-3p, and HSD11B2 expression levels in normal placental tissues and PE placental tissues were defined. HTR-8/SVneo cells were transfected to determine the effects of PVT1, miR-24-3p, and HSD11B2 on the growth of HTR-8/SVneo cells. The relationships among PVT1/ miR-24-3p/HSD11B2 in HTR-8/SVneo cells were identified. PVT1 and HSD11B2 were downregulated, while miR-24-3p was upregulated in the placenta of PE. Upregulated/ downregulated PVT1 promoted/impeded the growth of human placental trophoblast (HTR-8/SVneo) cells in PE. Restored/knocked down miR-24-3p impeded/enhanced the growth of HTR-8/SVneo cells in PE. PVT1 inhibited miR-24-3p to mediate HSD11B2.

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Fibrinogen-Like Protein 2-Associated Transcriptional and Histopathological Features of Immunological Preeclampsia

Abstract: Supplemental Digital Content is available in the text.

Cited by 7 publications

References 33 publications

A comparison of rat models that best mimic immune-driven preeclampsia in humans

A comparison of rat models that best mimic immune-driven preeclampsia in humans

Analysis of Proteomic Characteristics of Peripheral Blood in Preeclampsia and Study of Changes in Fetal Arterial Doppler Parameters Based on Magnetic Nanoparticles

Long noncoding RNA PVT1 accelerates the growth of placental trophoblasts in preeclampsia through the microRNA‐24‐3p/HSD11B2 axis

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