TREM-1 amplifies trophoblastic inflammation via activating NF-κB pathway during preeclampsia

Li, Xuanxuan; Lv, Dan; He, Mengzhou; Sun, Yanan; Lin, Xingguang; Fan, Yu; Yang, Meitao; Xu, Heze; Zhang, Xiaolei; Zhang, Yanling; Beejadhursing, Rajluxmee; Li, Fanfan; Deng, Dan

doi:10.1016/j.placenta.2021.09.016

Cited by 7 publications

(6 citation statements)

References 41 publications

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“…Additionally, TREM1, which is a myeloid cell surface receptor that is expressed on the surfaces of neutrophils, monocytes, and macrophages, amplifies inflammatory responses in coordination with classical pattern recognition receptors (PRRS), such as toll-like receptor (TLR) family and nod-like receptor (NLR) family. Xie et al reported that during PE, TREM1 amplifies trophoblastic inflammation via the activation of the NF- κ B pathway [ 36 ]. Additionally, studies on SLCO4A1 have been predominantly focused on microRNA and cancer.…”

Section: Discussionmentioning

confidence: 99%

Prediction of Differentially Expressed Genes and a Diagnostic Signature of Preeclampsia via Integrated Bioinformatics Analysis

Huang

Cai

et al. 2022

Disease Markers

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Background. Preeclampsia (PE), which has a high incidence rate worldwide, is a potentially dangerous syndrome to pregnant women and newborns. However, the exact mechanism of its pathogenesis is still unclear. In this study, we used bioinformatics analysis to identify hub genes, establish a logistic model, and study immune cell infiltration to clarify the physiopathogenesis of PE. Methods. We downloaded the GSE75010 and GSE10588 datasets from the GEO database and performed weighted gene coexpression network analysis (WGCNA) as well as Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. The online search tool for the retrieval of interacting genes and Cytoscape software were used to identify hub genes, which were then used to establish a logistic model. We also analyzed immune cell infiltration. Finally, we verified the expression of the genes included in the predictive model via RT-PCR. Results. A total of 100 and 212 differently expressed genes were identified in the GSE75010 and GSE10588 datasets, respectively, and after overlapping with WGCNA results, 17 genes were identified. KEGG and GO analyses further indicated the involvement of these genes in bioprocesses, such as gonadotropin secretion, immune cell infiltration, and the SMAD and MAPK pathways. Additionally, protein-protein interaction network analysis identified 10 hub genes, six (FLT1, FLNB, FSTL3, INHA, TREM1, and SLCO4A1) of which were used to establish a logistic model for PE. RT-PCR analysis also confirmed that, except FSTL3, these genes were upregulated in PE. Our results also indicated that macrophages played the most important role in immune cell infiltration in PE. Conclusion. This study identified 10 hub genes in PE and used 6 of them to establish a logistic model and also analyzed immune cell infiltration. These findings may enhance the understanding of PE and enable the identification of potential therapeutic targets for PE.

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Section: Discussionmentioning

confidence: 99%

Prediction of Differentially Expressed Genes and a Diagnostic Signature of Preeclampsia via Integrated Bioinformatics Analysis

Huang

Cai

et al. 2022

Disease Markers

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“…But human monocyte/macrophages did not depend on PGE2 for up-regulation of TREM-1 [24]. TREM-1, as an inflammation amplifier, induced multiple pro-inflammatory cytokines release [18,26].…”

Section: Discussionmentioning

confidence: 92%

"Research on the Molecular Mechanism of Combination Triptolide with Dexamethasone in Treatment of Rheumatoid Arthritis based on Bioinformatics Analysis"

Xiao

2023

BJSTR

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“…In contrast, we observed that IL-12 p70 was decreased after both six (1.4-fold, p < 0.009) and four days (1.2-fold, p < 0.02) of eCig treatment ( Figure 3 C). TREM-1 is a molecule that has been implicated in the propagation of the inflammatory response that is upregulated during PE [ 31 ]. Placental Trem-1 was increased following four days of SHS treatment (1.4-fold, p < 0.002) and with six days of eCig treatment (1.6-fold, p < 0.0001, Figure 3 D).…”

Section: Resultsmentioning

confidence: 99%

Different Lengths of Gestational Exposure to Secondhand Smoke or e-Cigarette Vapor Induce the Development of Placental Disease Symptoms

Kirkham,

Cooper,

Broberg

et al. 2024

Cells

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Exposure to cigarette smoke is known to induce disease during pregnancy. Recent evidence showed that exposure to secondhand smoke (SHS) negatively impacts fetal and placental weights, leading to the development of intrauterine growth restriction (IUGR). Electronic cigarettes (eCigs) represent a phenomenon that has recently emerged, and their use is also steadily rising. Even so, the effects of SHS or eCigs during gestation remain limited. In the present study, we wanted to characterize the effects of SHS or eCig exposure at two different important gestational points during mouse pregnancy. C57/Bl6 mice were exposed to SHS or eCigs via a nose-only delivery system for 4 days (from 14.5 to 17.5 gestational days (dGA) or for 6 days (from 12.5 dGA to 17.5 dGA)). At the time of necropsy (18.5 dGA), placental and fetal weights were recorded, maternal blood pressure was determined, and a dipstick test to measure proteinuria was performed. Placental tissues were collected, and inflammatory molecules in the placenta were identified. Treatment with SHS showed the following: (1) a significant decrease in placental and fetal weights following four days of exposure, (2) higher systolic and diastolic blood pressure following six days of exposure, and (3) increased proteinuria after six days of exposure. Treatment with eCigs showed the following: (1) a significant decrease in placental weight and fetal weight following four or six days of exposure, (2) higher systolic and diastolic blood pressure following six days of exposure, and (3) increased proteinuria after six days of exposure. We also observed different inflammatory markers associated with the development of IUGR or PE. We conclude that the detrimental effects of SHS or eCig treatment coincide with the length of maternal exposure. These results could be beneficial in understanding the long-term effects of SHS or eCig exposure in the development of placental diseases.

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TREM-1 amplifies trophoblastic inflammation via activating NF-κB pathway during preeclampsia

Cited by 7 publications

References 41 publications

Prediction of Differentially Expressed Genes and a Diagnostic Signature of Preeclampsia via Integrated Bioinformatics Analysis

Prediction of Differentially Expressed Genes and a Diagnostic Signature of Preeclampsia via Integrated Bioinformatics Analysis

"Research on the Molecular Mechanism of Combination Triptolide with Dexamethasone in Treatment of Rheumatoid Arthritis based on Bioinformatics Analysis"

Different Lengths of Gestational Exposure to Secondhand Smoke or e-Cigarette Vapor Induce the Development of Placental Disease Symptoms

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