Hydrogen peroxide-mediated oxidative stress induces inflammasome activation in term human placental explants

Nunes, Priscila Rezeck; Peraçoli, Maria Terezinha Serrão; Romao‐Veiga, Mariana; Matias, Mariana Letícia; Ribeiro, Vanessa Rocha; Fernandes, Célio Júnior da Costa; Peraçoli, José Carlos; Rodrigues, José Ricardo Paciência

doi:10.1016/j.preghy.2018.07.006

Cited by 17 publications

(14 citation statements)

References 50 publications

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“…In a previous study published by our research group, we observed that some markers of oxidative stress, such as superoxide dismutase (SOD) and catalase are altered at high concentrations of hydrogen peroxide confirming that H 2 O 2 induces oxidative stress on placental explants and demonstrated that this stress involves inflammasome activation [53].…”

Section: Autophagy and Inflammasomessupporting

confidence: 69%

Autophagy in Preeclampsia

Nunes¹,

Oliveira²,

Veiga³

et al. 2019

Prediction of Maternal and Fetal Syndrome of Preeclampsia

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Autophagy may be involved in gestation complicated by preeclampsia (PE) due to the presence of placental lesions caused by hypoxia at fetomaternal interphase. Autophagy is a lysosomal degradation pathway, removing protein aggregates and organelles damaged and thereby maintaining cell integrity. In preeclampsia, deficient myometrial penetration by extravillous cytotrophoblast occurs during the first trimester of pregnancy, leading to placental insufficiency. Several placental functions, like nutrient and oxygen input to the fetus during pregnancy, might benefit or even rely on autophagy and related material recycling within the cell. Deficiency in autophagy mechanism has been correlated to inflammatory responses. Autophagy is regulated during placentation and appears to be a possible factor in the development of preeclampsia. In this chapter, we intend to discuss evidence on autophagy pathway in pregnancy and the crosstalk between autophagy and inflammation in preeclampsia.

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Section: Autophagy and Inflammasomessupporting

confidence: 69%

Autophagy in Preeclampsia

Nunes¹,

Oliveira²,

Veiga³

et al. 2019

Prediction of Maternal and Fetal Syndrome of Preeclampsia

View full text Add to dashboard Cite

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“…Furthermore, this effect was abolished by glibenclamide, an NLRP3 inhibitor [ 45 ]. Another, similarly designed, study confirmed that NLRP3 is activated by cholesterol, ROS, MSU, hyaluronan, and high glucose concentrations [ 45 , 46 , 47 , 48 , 49 ]. These findings led to the creation of the NLRP3 crystal-induced activation theory, where MSU, alum, silica, asbestos, β-amyloid, cholesterol crystals, and calcium crystals, induces NLRP3 inflammasome activation [ 6 , 45 ].…”

Section: Nlrp3 Activators In Pe and Pihmentioning

confidence: 87%

The NLRP3 Inflammasome Role in the Pathogenesis of Pregnancy Induced Hypertension and Preeclampsia

Socha

Malinowski

Puk

et al. 2020

Cells

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Pregnancy-induced hypertension and preeclampsia are associated with significant maternal and fetal mortality. A better understanding of these diseases, delineation of molecular pathomechanism, and efficient treatment development are some of the most urgent tasks in obstetrics and gynecology. Recent findings indicate the crucial role of inflammation in the development of hypertension and preeclampsia. Although the mechanism is very complex and needs further explanation, it appears that high levels of cholesterol, urate, and glucose activates NLRP3 inflammasome, which produces IL-1β, IL-18, and gasdermin D. Production of these proinflammatory chemokines is the beginning of a local and general inflammation, which results in sympathetic outflow, angiotensin II production, proteinuria, hemolysis, liver damage, immunothrombosis, and coagulopathy. The NLRP3 inflammasome is a critical complex in the mediation of the inflammatory response, which makes it crucial for the development of pregnancy-induced hypertension and preeclampsia, as well as its complications, such as placental abruption and HELLP (hemolysis, elevated liver enzymes, and low platelets) syndrome. Herein, the presented article delineates molecular mechanisms of these processes, indicating directions of future advance.

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“…Recent studies by Nunes et al reported that alterations in STB functions as a consequence of the imbalance between pro-and antioxidant properties may also cause cellular stress and injury to activate inflammasomes [64]. Although the molecular mechanism involved in placental inflammasome activation in PE is largely unknown, it is possible that the inappropriate inflammatory response observed in PE may have its origin in the placenta.…”

Section: Activation Of Inflammasomes In Preeclampsia-affected Pregnanmentioning

confidence: 99%

Inflammasomes—A Molecular Link for Altered Immunoregulation and Inflammation Mediated Vascular Dysfunction in Preeclampsia

Murthi

Pinar

Dimitriadis

et al. 2020

IJMS

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Preeclampsia (PE) is a pregnancy-specific multisystem disorder and is associated with maladaptation of the maternal cardiovascular system and abnormal placentation. One of the important characteristics in the pathophysiology of PE is a dysfunction of the placenta. Placental insufficiency is associated with poor trophoblast uterine invasion and impaired transformation of the uterine spiral arterioles to high capacity and low impedance vessels and/or abnormalities in the development of chorionic villi. Significant progress in identifying potential molecular targets in the pathophysiology of PE is underway. The human placenta is immunologically functional with the trophoblast able to generate specific and diverse innate immune-like responses through their expression of multimeric self-assembling protein complexes, termed inflammasomes. However, the type of response is highly dependent upon the stimuli, the receptor(s) expressed and activated, the downstream signaling pathways involved, and the timing of gestation. Recent findings highlight that inflammasomes can act as a molecular link for several components at the syncytiotrophoblast surface and also in maternal blood thereby directly influencing each other. Thus, the inflammasome molecular platform can promote adverse inflammatory effects when chronically activated. This review highlights current knowledge in placental inflammasome expression and activity in PE-affected pregnancies, and consequently, vascular dysfunction in PE that must be addressed as an interdependent interactive process.

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Hydrogen peroxide-mediated oxidative stress induces inflammasome activation in term human placental explants

Cited by 17 publications

References 50 publications

Autophagy in Preeclampsia

Autophagy in Preeclampsia

The NLRP3 Inflammasome Role in the Pathogenesis of Pregnancy Induced Hypertension and Preeclampsia

Inflammasomes—A Molecular Link for Altered Immunoregulation and Inflammation Mediated Vascular Dysfunction in Preeclampsia

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