Early pregnancy protein multiplex screening reflects circulating and urinary divergences associated with the development of preeclampsia

Martínez‐Fierro, Margarita L.; Rosa, Claudia Castruita-De la; Cardiel-Hernandez, Rosa M; Espinoza-Juarez, Marcela A.; Delgado‐Enciso, Iván; Castañeda-Lopez, Maria E.; Cardenas-Vargas, Edith; Trejo‐Vazquez, Fabiola; Sotelo-Ham, Elma Ivonne; Castañeda‐Miranda, Rodrigo; Cid-Baez, Miguel A; Ortiz-Rodríguez, J.M.; Solís-Sánchez, Luis Octavio; Aviles, Angelica Garcia; Ortiz-Castro, Yolanda

doi:10.1080/10641955.2017.1411946

Cited by 15 publications

(7 citation statements)

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“…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

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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.

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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

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Section: Methodsmentioning

confidence: 99%

“…This was a retrospective nested cohort case-control study in which the participants were drawn from a cohort of pregnant women who were followed from the first trimester to delivery as part of a screening study for adverse pregnancy outcomes, in Zacatecas Mexico [20,21] (Figure 1). which quantified miRNA profiles in first-trimester serum samples from pregnant women who subsequently developed early PE, significant miRNA signatures were not identified [13].…”

Section: Patients and Study Designmentioning

confidence: 99%

“…This was a retrospective nested cohort case-control study in which the participants were drawn from a cohort of pregnant women who were followed from the first trimester to delivery as part of a screening study for adverse pregnancy outcomes, in Zacatecas Mexico [20,21] (Figure 1). Sixteen women who later developed PE (WWD-PE) during the follow-up period were selected and matched to 18 women in the cohort who had healthy pregnancies without complications (controls).…”

Section: Patients and Study Designmentioning

confidence: 99%

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Analysis of Circulating microRNA Signatures and Preeclampsia Development

Martínez‐Fierro

2021

Cells

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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.

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“…However, the role of the family history of hypertension as an independent risk factor of pregnancy-induced hypertension (PIH) has not been clearly established [ 4 , 8 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 ]. Only the Society of Obstetricians and Gynaecologists of Canada (SOGC) 2014 guidelines list a family history of early cardiovascular disease among the risk factors for preeclampsia (PE) that determine the use of aspirin prophylaxis, in contrast to the guidelines of other scientific societies [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

The Association of Familial Hypertension and Risk of Gestational Hypertension and Preeclampsia

Lewandowska

2021

IJERPH

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It has not been established how history of hypertension in the father or mother of pregnant women, combined with obesity or smoking, affects the risk of main forms of pregnancy-induced hypertension. A cohort of 912 pregnant women, recruited in the first trimester, was assessed; 113 (12.4%) women developed gestational hypertension (GH), 24 (2.6%) developed preeclampsia (PE) and 775 women remained normotensive (a control group). Multiple logistic regression was used to calculate adjusted odds ratios (AOR) (and 95% confidence intervals) of GH and PE for chronic hypertension in the father or mother of pregnant women. Some differences were discovered. (1) Paternal hypertension (vs. absence of hypertension in the family) was an independent risk factor for GH (AOR-a = 1.98 (1.2–3.28), p = 0.008). This odds ratio increased in pregnant women who smoked in the first trimester (AOR-a = 4.71 (1.01–21.96); p = 0.048) or smoked before pregnancy (AOR-a = 3.15 (1.16–8.54); p = 0.024), or had pre-pregnancy overweight (AOR-a = 2.67 (1.02–7.02); p = 0.046). (2) Maternal hypertension (vs. absence of hypertension in the family) was an independent risk factor for preeclampsia (PE) (AOR-a = 3.26 (1.3–8.16); p = 0.012). This odds ratio increased in the obese women (AOR-a = 6.51 (1.05–40.25); p = 0.044) and (paradoxically) in women who had never smoked (AOR-a = 5.31 (1.91–14.8); p = 0.001). Conclusions: Chronic hypertension in the father or mother affected the risk of preeclampsia and gestational hypertension in different ways. Modifiable factors (overweight/obesity and smoking) may exacerbate the relationships in question, however, paradoxically, beneficial effects of smoking for preeclampsia risk are also possible. Importantly, paternal and maternal hypertension were not independent risk factors for GH/PE in a subgroup of women with normal body mass index (BMI).

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Early pregnancy protein multiplex screening reflects circulating and urinary divergences associated with the development of preeclampsia

Abstract: The proteins sEGFR, HGF, ANG-2, sFASL, IL-6, PLGF, VEGF-A, PRL, TGF-α FGF-b, sHER2/Neu sIL-6Rα, ENG, uPA, and insulin-like growth factor binding protein 1 (IGFBP-1), were predictive of the development of preeclampsia and their use as markers for this disease should be considered.

Cited by 15 publications

References 47 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

The Association of Familial Hypertension and Risk of Gestational Hypertension and Preeclampsia

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