Analysis of association of clinical aspects and <i>IL1B</i> tagSNPs with severe preeclampsia

Galvão, Larissa Paes Leme; Menezes, Filipe Emanuel Fonseca; Mendonça, Caio Menezes Machado de; Barreto, Íkaro Daniel de Carvalho; Alvim-Pereira, Cláudia Cristina; Alvim-Pereira, Fabiano; Gurgel, Ricardo Queiróz

doi:10.3109/10641955.2015.1116554

Cited by 14 publications

(11 citation statements)

References 25 publications

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“…IL-1β gene polymorphisms have been associated with preeclampsia 62,63 , preterm birth 75 , and recurrent pregnancy loss 76 . In their Brazilian study, Leme et al 77 , have found an association of preeclampsia risk with the IL-1β rs1143630 T allele, while Pontillo et al 78 , who also conducted their study in Brazil, have found no association of IL1β rs1143634 with preeclampsia risk, a finding similar to that of other studies 79 . The -511 C/T polymorphism in the IL-1β gene promoter region is implicated in the differential production of cytokines.…”

Section: Discussionsupporting

confidence: 60%

Genetic markers for preeclampsia in Peruvian women

et al. 2021

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Background: Preeclampsia is a multiorgan disorder associated with maternal and perinatal morbi-mortality. In Peru, incidence is 10% and accounts for 22% of maternal deaths. Genome and genetic epidemiological studies have found an association between preeclampsia and genetic polymorphisms. Objective: To determine the association of the vascular endothelial growth factor (VEGF) +936 C/T and +405 G/C, interleukine-6 (IL-6) -174 G/C, IL-1β-511 C/T, Apo A-1-75 G/A, Apo B-100 2488 C/T (Xbal) polymorphisms with preeclampsia in pregnant Peruvian women. Methods: Were included preeclamptic and healthy (control) pregnant women. Maternal blood samples were subjected to DNA extraction, and molecular genetic analysis was conducted using the PCR-RFLP technique and following a specific protocol for each gene. Allele and genotypic frequencies in the cases and controls were compared. Results: No association was found between the VEGF+936C/T and VEGF+405 polymorphisms and preeclampsia. The frequencies of the GG genotypes and the G allele of the -174 G/C polymorphism in the IL6 gene in preeclamptic and controls showed significant differences, with higher frequencies in cases. For the -511 C/T polymorphism of the IL-1β gene, no significant differences were found in the frequencies of TT genotypes compared with CT+CC. The genotypes and alleles of the Apo-A1-75 G/A and Apo-B100 Xbal variants showed no significant differences between cases and controls. Conclusion: No association was found between the studied genetic markers and preeclampsia. However, in the -174G/C polymorphism of the IL-6 gene, significant differences were found mainly in the GG genotype and G allele.

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Section: Discussionsupporting

confidence: 60%

Genetic markers for preeclampsia in Peruvian women

et al. 2021

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“…A possible association between SNPs in IL1B was investigated in Brazilian women with severe PE. In this study, the “rs1143630 T” allele was associated with PE (Leme Galvão et al, 2016). In a Maya-Mestizo population sample, no association between TNFA (−308G/A, −850C/T) SNPs and PE was observed (Canto-Cetina et al, 2007).…”

Section: Genetic Studies In Latin-american Populationsmentioning

confidence: 59%

Genetic Variants in Preeclampsia: Lessons From Studies in Latin-American Populations

Michita

Kaminski

2018

Front. Physiol.

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Placental vascularization is a tightly regulated physiological process in which the maternal immune system plays a fundamental role. Vascularization of the maternal-placental interface involves a wide range of mechanisms primarily orchestrated by the fetal extravillous trophoblast and maternal immune cells. In a healthy pregnancy, an immune cross-talk between the mother and fetal cells results in the secretion of immunomodulatory mediators, apoptosis of specific cells, cellular differentiation/proliferation, angiogenesis, and vasculogenesis, altogether favoring a suitable microenvironment for the developing embryo. In the context of vasculopathy underlying common pregnancy disorders, it is believed that inefficient invasion of extravillous trophoblast cells in the endometrium leads to a poor placental blood supply, which, in turn, leads to decreased secretion of angiogenic factors, hypoxia, and inflammation commonly associated with preterm delivery, intrauterine growth restriction, and preeclampsia. In this review, we will focus on studies published by Latin American research groups, providing an extensive review of the role of genetic variants from candidate genes involved in a broad spectrum of biological processes underlying the pathophysiology of preeclampsia. In addition, we will discuss how these studies contribute to fill gaps in the current understanding of preeclampsia. Finally, we discuss some trending topics from important fields associated with pregnancy vascular disorders (e.g., epigenetics, transplantation biology, and non-coding RNAs) and underscore their possible implications in the pathophysiology of preeclampsia. As a result, these efforts are expected to give an overview of the extent of scientific research produced in Latin America and encourage multicentric collaborations by highlighted regional research groups involved in preeclampsia investigation.

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“…These opposing signals may provide an explanation for the variation in fetal outcomes observed in pregnancies complicated by obesity. IL-1β appears to be consistently associated with hypertensive disorders such as preeclampsia (Kalinderis et al 2011; Dong and Yin 2014; Leme Galvão et al 2016) and may be predictive of future disease in early to mid pregnancy (Siljee et al 2013; Taylor et al 2016). Enhanced placental secretion may be the primary source of circulating of IL-1β (Amash et al 2012).…”

Section: Obstetric Complications Associated With Maternal Obesitymentioning

confidence: 99%

Effects of maternal obesity on placental function and fetal development

2017

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Obesity has reached epidemic proportions and pregnancies in obese mothers have increased risk for complications including gestational diabetes, hypertensive disorders, preterm birth and caesarian section. Children born to obese mothers are at increased risk of obesity and metabolic disease and are susceptible to develop neuropsychiatric and cognitive disorders. Changes in placental function not only play a critical role in the development of pregnancy complications but may also be involved in linking maternal obesity to long-term health risks in the infant. Maternal adipokines i.e., interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), leptin and adiponectin link maternal nutritional status and adipose tissue metabolism to placental function. Adipokines and metabolic hormones have direct impact on placental function by modulating placental nutrient transport. Nutrient delivery to the fetus is regulated by a complex interaction between insulin signaling, cytokine profile and insulin responsiveness, which is modulated by adiponectin and IL-1β. In addition, obese pregnant women are at risk for hypertension and preeclampsia with reduced placental vascularity and blood flow, which would restrict placental nutrient delivery to the developing fetus. These sometimes opposing signals regulating placental function may contribute to the diversity of short and long-term outcomes observed in pregnant obese women. This review focuses on the changes in adipokines and obesity-related metabolic hormones, how these factors influence placental function and fetal development to contribute to long-term metabolic and behavioral consequences of children born to obese mothers.

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Analysis of association of clinical aspects and IL1B tagSNPs with severe preeclampsia

Cited by 14 publications

References 25 publications

Genetic markers for preeclampsia in Peruvian women

Genetic markers for preeclampsia in Peruvian women

Genetic Variants in Preeclampsia: Lessons From Studies in Latin-American Populations

Effects of maternal obesity on placental function and fetal development

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