Evidence map›Paper›PMID 39587640›Full record

ArticleBiology direct2024

miR-155 mediated regulation of PKG1 and its implications on cell invasion, migration, and apoptosis in preeclampsia through NF-κB pathway.

Xiaohua Luo, Xiaopei Guo, Ningning Chen, Rui Peng, Ci Pan, Zhuyin Li, Bing Zhao, Ruonan Ji, Siyu Li

Abstract read
In one paragraph

Article in Biology direct, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Xiaohua LuoDepartment of Obstetrics and Gynaecology, The Third Affiliated Hospital of Zhengzhou University, No.7 Kangfuqian Street, Erqi District, Zhengzhou, 450052, Henan, China. luoxiaohua620@zzu.edu.cn.
Xiaopei GuoDepartment of Obstetrics and Gynaecology, The Third Affiliated Hospital of Zhengzhou University, No.7 Kangfuqian Street, Erqi District, Zhengzhou, 450052, Henan, China.
Ningning ChenDepartment of Obstetrics and Gynaecology, The Third Affiliated Hospital of Zhengzhou University, No.7 Kangfuqian Street, Erqi District, Zhengzhou, 450052, Henan, China.
Rui PengScientific Research Department, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, Henan, China.
Ci PanDepartment of Obstetrics and Gynaecology, The Third Affiliated Hospital of Zhengzhou University, No.7 Kangfuqian Street, Erqi District, Zhengzhou, 450052, Henan, China.
Zhuyin LiDepartment of Obstetrics and Gynaecology, The Third Affiliated Hospital of Zhengzhou University, No.7 Kangfuqian Street, Erqi District, Zhengzhou, 450052, Henan, China.
Bing ZhaoDepartment of Obstetrics and Gynaecology, The Third Affiliated Hospital of Zhengzhou University, No.7 Kangfuqian Street, Erqi District, Zhengzhou, 450052, Henan, China.
Ruonan JiDepartment of Obstetrics and Gynaecology, The Third Affiliated Hospital of Zhengzhou University, No.7 Kangfuqian Street, Erqi District, Zhengzhou, 450052, Henan, China.
Siyu LiDepartment of Obstetrics and Gynaecology, The Third Affiliated Hospital of Zhengzhou University, No.7 Kangfuqian Street, Erqi District, Zhengzhou, 450052, Henan, China.

Funding

Health Commission of Henan Province SBGJ202302083
6 · The paper itself

Abstract

backgroundPreeclampsia (PE) is a severe pregnancy complication characterized by complex molecular interactions. Understanding these interactions is crucial for developing effective therapeutic strategies.

methodsThis study applies a pharmacometabolomics approach to explore the roles of miR-155 and PKG1 in PE, focusing on the regulatory influence of the NF-κB signaling pathway. Blood metabolomic profiles were analyzed, and bioinformatics tools, IHC staining, Western blot (WB) analysis, and immunofluorescence (IF) localization were employed to determine the expression and function of miR-155 and PKG1. Cell invasion, migration, proliferation, and apoptosis assays were conducted to assess miR-155's modulation of PKG1. Additionally, RT-qPCR and WB analysis elucidated NF-κB-mediated regulation mechanisms.

resultsOur findings indicate significant metabolic alterations associated with miR-155 modulation of PKG1, with NF-κB acting as a critical upstream regulator. The study demonstrates that miR-155 affects cellular functions such as invasion, migration, proliferation, and apoptosis through PKG1 modulation. Furthermore, the NF-κB signaling pathway regulates miR-155 expression, contributing to the pathological processes of PE.

conclusionThis study provides a proof of concept for using pharmacometabolomics to understand the molecular mechanisms of PE, suggesting new therapeutic targets and advancing personalized medicine approaches. These insights highlight the potential of pharmacometabolomics to complement genomic and transcriptional data in disease characterization and treatment strategies, offering new avenues for therapeutic intervention in PE.

Indexed as

ApoptosisCell MovementCyclic GMP-Dependent Protein Kinase Type IMicroRNAsNF-kappa BPre-EclampsiaSignal TransductionAdultCell ProliferationFemaleHumansPregnancyCyclic GMP-Dependent Protein Kinase Type IMicroRNAsMIRN155 microRNA, humanNF-kappa BPRKG1 protein, humanCell behavior modulationmiR-155 regulationNF-κB signaling pathwayPKG1 expressionPreeclampsia

Identifiers

PMID39587640
PMCPMC11590512

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.