Plasma cancer biomarker multiplex screening and the risk of subsequent preeclampsia

Martínez‐Fierro, Margarita L.; Rosa, Claudia Castruita-Dela; Ortiz-Castro, Yolanda; Aceves-Medina, Maria C.; Vázquez-Castro, Rosbel; Delgado‐Enciso, Iván; Castañeda-Lopez, Maria E.

doi:10.1016/j.ijcard.2014.10.168

Cited by 11 publications

(9 citation statements)

References 12 publications

(12 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, due to the disturbed endothelial cell function in placental tissue in severe PE cases, the regulation of this imbalance may be not possible and it may explain the lower FGF2 serum concentrations observed in women with severe PE Hohlagschwandtner et al, 2002). The relationship between the circulating FGF2 concentration and PE development has been reported in other studies, in which a decrease in FGF2 plasma concentrations was observed at 16 WG in pregnant women who subsequently developed PE when they were compared with women with normotensive pregnancies (Martinez-Fierro et al, 2015;Martinez-Fierro et al, 2018b). Based on the above, we inferred that low FGF2 circulating concentrations could be due to the poor response of the FGF2 regulatory mechanism.…”

Section: Introductionsupporting

confidence: 82%

Fibroblast Growth Factor Type 2 (FGF2) Administration Attenuated the Clinical Manifestations of Preeclampsia in a Murine Model Induced by L-NAME

et al. 2021

Self Cite

View full text Add to dashboard Cite

Background: In preeclampsia, a hypertensive disorder of pregnancy, the poor remodeling of spiral arteries leads to placental hypoperfusion and ischemia, provoking generalized maternal endothelial dysfunction and, in severe cases, death. Endothelial and placental remodeling is important for correct pregnancy evolution and is mediated by cytokines and growth factors such as fibroblast growth factor type 2 (FGF2). In this study, we evaluated the effect of human recombinant FGF2 (rhFGF2) administration in a murine model of PE induced by NG-nitro-L-arginine methyl ester (L-NAME) to test if rhFGF2 administration can lessen the clinical manifestations of PE.Methods: Pregnant rats were administrated with 0.9% of NaCl (vehicle), L-NAME (60 mg/kg), FGF2 (666.6 ng/kg), L-NAME+FGF2 or L-NAME + hydralazine (10 mg/kg) from the 10th to 19th days of gestation. Blood pressure (BP), urine protein concentrations and anthropometric values both rat and fetuses were assessed. Histological evaluation of organs from rats delivered by cesarean section was carried out using hematoxylin and eosin staining.Results: A PE-like model was established, and it included phenotypes such as maternal hypertension, proteinuria, and fetal growth delay. Compared to the groups treated with L-NAME, the L-NAME + FGF2 group was similar to vehicle: the BP remained stable and the rats did not develop enhanced proteinuria. Both the fetuses and placentas from rats treated with L-NAME + FGF2 had similar values of weight and size compared with the vehicle.Conclusion: The intravenous administration of rhFGF2 showed beneficial and hypotensive effects, reducing the clinical manifestations of PE in the evaluated model.

show abstract

Section: Introductionsupporting

confidence: 82%

Fibroblast Growth Factor Type 2 (FGF2) Administration Attenuated the Clinical Manifestations of Preeclampsia in a Murine Model Induced by L-NAME

et al. 2021

Self Cite

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

“…Abnormal trophoblast implantation is tightly related to the proliferative and invasive capacities of trophoblastic cells [ 20 ]. Considering the molecular mechanisms involved during implantation, recent evidence suggests common links between PE and cancer progression pathways [ 20 , 27 , 28 , 29 ]. In agreement with these reports and with the findings regarding circulating PE-modulated members of the C19MC cluster (some of which are cancer-related) [ 30 ], the signaling pathways modeling results showed that in addition to cancer-related KEGG pathways, Wnt, MAPK, PI3K-Akt, ErbB, GnRH, VEGF, B/T cell receptors, and ubiquitin-mediated proteolysis signaling pathways, were the most commonly modulated by the miRNAs altered in WWD-PE in our study.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Analysis of Circulating microRNA Signatures and Preeclampsia Development

Martínez‐Fierro

2021

Cells

Self Cite

View full text Add to dashboard Cite

microRNAs are important regulators of cell processes and have been proposed as potential preeclampsia biomarkers. We evaluated serum microRNA expression profiling to identify microRNAs involved in preeclampsia development. Serum microRNA expression profiling was evaluated at 12, 16, and 20 weeks of gestation (WG), and at the time of preeclampsia diagnosis. Two groups were evaluated using TaqMan low-density array plates: a control group with 18 normotensive pregnant women and a case group with 16 patients who developed preeclampsia during the follow-up period. Fifty-three circulating microRNAs were differentially expressed between groups (p < 0.05). Compared with controls, hsa-miR-628-3p showed the highest relative quantity values (at 12 WG = 7.7 and at 20 WG = 3.45) and the hsa-miRs -151a-3p and -573 remained differentially expressed from 16 to 20 WG (p < 0.05). Signaling pathways including cancer-related, axon guidance, Neurotrophin, GnRH, VEGF, and B/T cell receptor, were most commonly altered. Further target gene prediction revealed that nuclear factor of activated T-cells 5 gene was included among the transcriptional targets of preeclampsia-modulated microRNAs. Specific microRNAs including hsa-miRs -628-3p, -151a-3p, and -573 were differentially expressed in serum of pregnant women before they developed preeclampsia compared with controls and their participation in the preeclampsia development should be considered.

show abstract

“…In PE, several researchers have investigated the utility of clinical variables, maternal characteristics, and biophysical and biochemical markers obtained early during gestation, to develop models for predicting PE (occurrence and severity). [77][78][79][80][81][82][83][84] The variables that have been modeled include maternal age, body mass index (BMI), height, parity, blood pressure, hematocrit count, smoking, previous miscarriage, family history of high blood pressure, ultrasound variables such as mean arterial pressure (MAP) and uterine artery pulsatility index (PI), [85][86][87][88] first-trimester urine and serum metabolomic profiles, 89 and biochemical markers such as maternal plasma or serum levels of placental protein-13, PGF, pregnancy-associated plasma protein-A, P-selectin, pentraxin-3, activin-A, inhibin-A, and sENG. 90 The prediction efficacy of each model may be compared considering the specificity and sensitivity values and/or with the area under the curve.…”

Section: Othersmentioning

confidence: 99%

Current model systems for the study of preeclampsia

Martínez‐Fierro

Hernandez-Delgadillo

Flores‐Morales

et al. 2018

Exp Biol Med (Maywood)

View full text Add to dashboard Cite

Preeclampsia (PE) is a pregnancy complex disease, distinguished by high blood pressure and proteinuria, diagnosed after the 20th gestation week. Depending on the values of blood pressure, urine protein concentrations, symptomatology, and onset of disease there is a wide range of phenotypes, from mild forms developing predominantly at the end of pregnancy to severe forms developing in the early stage of pregnancy. In the worst cases severe forms of PE could lead to systemic endothelial dysfunction, eclampsia, and maternal and/or fetal death. Worldwide the fetal morbidity and mortality related to PE is calculated to be around 8% of the total pregnancies. PE still being an enigma regarding its etiology and pathophysiology, in general a deficient trophoblast invasion during placentation at first stage of pregnancy, in combination with maternal conditions are accepted as a cause of endothelial dysfunction, inflammatory alterations and appearance of symptoms. Depending on the PE multifactorial origin, several in vitro, in vivo, and in silico models have been used to evaluate the PE pathophysiology as well as to identify or test biomarkers predicting, diagnosing or prognosing the syndrome. This review focuses on the most common models used for the study of PE, including those related to placental development, abnormal trophoblast invasion, uteroplacental ischemia, angiogenesis, oxygen deregulation, and immune response to maternal-fetal interactions. The advances in mathematical and computational modeling of metabolic network behavior, gene prioritization, the protein-protein interaction network, the genetics of PE, and the PE prediction/classification are discussed. Finally, the potential of these models to enable understanding of PE pathogenesis and to evaluate new preventative and therapeutic approaches in the management of PE are also highlighted. Impact statement This review is important to the field of preeclampsia (PE), because it provides a description of the principal in vitro, in vivo, and in silico models developed for the study of its principal aspects, and to test emerging therapies or biomarkers predicting the syndrome before their evaluation in clinical trials. Despite the current advance, the field still lacking of new methods and original modeling approaches that leads to new knowledge about pathophysiology. The part of in silico models described in this review has not been considered in the previous reports.

show abstract

Plasma cancer biomarker multiplex screening and the risk of subsequent preeclampsia

Cited by 11 publications

References 12 publications

Fibroblast Growth Factor Type 2 (FGF2) Administration Attenuated the Clinical Manifestations of Preeclampsia in a Murine Model Induced by L-NAME

Fibroblast Growth Factor Type 2 (FGF2) Administration Attenuated the Clinical Manifestations of Preeclampsia in a Murine Model Induced by L-NAME

Analysis of Circulating microRNA Signatures and Preeclampsia Development

Current model systems for the study of preeclampsia

Contact Info

Product

Resources

About