Induction of systemic inflammation by hyaluronan and hsp70 in women with pre-eclampsia

Romao‐Veiga, Mariana; Matias, Mariana Letícia; Ribeiro, Vanessa Rocha; Nunes, Priscila Rezeck; Borges, Vera Therezinha Medeiros; Peraçoli, José Carlos; Peraçoli, Maria Terezinha Serrão

doi:10.1016/j.cyto.2018.02.007

Cited by 37 publications

(23 citation statements)

References 34 publications

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“…The results of the present study show that monocytes from preeclamptic women are endogenously activated and may play a role in the systemic inflammatory response already described in PE [26,27]. Compared with NT pregnant women, basal gene expression of NLRP1 and NLRP3 inflammasomes, the TLR4/NF-κB pathway and pro-inflammatory cytokines were significantly increased in monocytes from preeclamptic women, findings that highlight the inflammatory profile of these cells.…”

Section: Discussionsupporting

confidence: 71%

Silibinin Downregulates the NF-κB Pathway and NLRP1/NLRP3 Inflammasomes in Monocytes from Pregnant Women with Preeclampsia

et al. 2019

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Preeclampsia (PE) is a human pregnancy-specific syndrome with abnormal activation of cells from the innate immune system. The present study evaluated whether silibinin (SB) treatment of monocytes from preeclamptic women could modulate NLRP1 and NLRP3 inflammasomes as well as TLR4/NF-κB pathway activation. Peripheral blood monocytes from 20 preeclamptic and 20 normotensive (NT) pregnant women, as well as the THP-1 cell line, were cultured with or without monosodium urate (MSU) or SB. NLRP1, NLRP3, Caspase-1, TLR4, MyD88, NF-κB, IL-1β, IL-18, TNF-α and IL-10 gene expression by monocytes was analysed by quantitative real-time polymerase chain reaction (qPCR), while inflammatory cytokine production and p65NF-κB activity were determined by enzyme-linked immunosorbent assays (ELISAs). TLR4/MyD88/NF-κB and NLRP1/NLRP3 inflammasomes pathways in THP-1 cells were evaluated by flow cytometry and western blot respectively. Compared with NT women, monocytes from preeclamptic women showed The Ethics Committee of the Botucatu Medical School approved the study (protocol number 2.333.216)higher endogenous activation of NLRP1/NLRP3 inflammasomes and the TLR4/NF-κB pathway as well as higher gene and protein expression of IL-1β, IL-18 and TNF-α, and lower expression of IL-10. Monocyte stimulation with MSU increased inflammation-related genes as well as NF-κB activity. In vitro, SB treatment of monocytes from preeclamptic women reduced the basal activation of these cells by decreasing NLRP1/NLRP3 inflammasomes and p65NF-κB activity. THP-1 cells exhibited a similar immunological response profile to monocytes from preeclamptic women when cultured with or without MSU or SB. These results suggest uric acid participates in the systemic inflammatory response characteristic of preeclampsia and that in vitro SB treatment can modulate the sterile inflammation established in monocytes from preeclamptic women.

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Section: Discussionsupporting

confidence: 71%

Silibinin Downregulates the NF-κB Pathway and NLRP1/NLRP3 Inflammasomes in Monocytes from Pregnant Women with Preeclampsia

et al. 2019

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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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“…Excessive inflammation causes placental damage, placental development abnormalities, systemic endothelial system activation, and lease of antiangiogenic factors and thus leads to preeclampsia (Cornelius, 2018;I et al, 2017;Romao-Veiga et al, 2018). Accumulated data have Sakai, & Sasaki, 2007).…”

Section: Discussionmentioning

confidence: 99%

MiRNA‐548c‐5p downregulates inflammatory response in preeclampsia via targeting PTPRO

Wang

et al. 2018

Journal Cellular Physiology

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Preeclampsia is a serious complication of pregnancy and leads to maternal hypertension and proteinuria. It remains a major health problem for mothers and babies across the world due to high maternal and fetal morbidity and mortality. Accumulated data have implicated the critical role of microRNA in preeclampsia. However, to date, the role of miR‐548c‐5p in preeclampsia remains vaguely understood. In this study, we first elucidate the role of miR‐548c‐5p and its underlying molecular mechanism in preeclampsia. Compared with healthy controls, miR‐548c‐5p was obviously downregulated in serum exosomes and placental mononuclear cells in patients with preeclampsia. Nonetheless, PTPRO was significantly upregulated and negatively associated with miR‐548c‐5p in placental mononuclear cells in patients with preeclampsia. PTPRO was a target of miR‐548c‐5p. PTPRO was downregulated in the miR‐548c‐5p‐overexpressed macrophages. In addition, miR‐548c‐5p could inhibit the proliferation and activation of LPS‐stimulated macrophages, as evidenced by decreased levels of inflammatory cytokines (IL‐12 and TNF‐α) and less nuclear translocation of pNF‐κB in pTHP1 cells. MiR‐548c‐5p acts as an anti‐inflammatory factor in preeclampsia. The axis of miR‐548c‐5p/PTPRO/NF‐κB may provide novel targets for the diagnosis and treatment of preeclampsia.

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Induction of systemic inflammation by hyaluronan and hsp70 in women with pre-eclampsia

Cited by 37 publications

References 34 publications

Silibinin Downregulates the NF-κB Pathway and NLRP1/NLRP3 Inflammasomes in Monocytes from Pregnant Women with Preeclampsia

Silibinin Downregulates the NF-κB Pathway and NLRP1/NLRP3 Inflammasomes in Monocytes from Pregnant Women with Preeclampsia

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

MiRNA‐548c‐5p downregulates inflammatory response in preeclampsia via targeting PTPRO

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