Evidence map›Paper›PMID 29280536›Full record

ArticleNephrology (Carlton, Vic.)2019

Screening of genes involved in epithelial-mesenchymal transition and differential expression of complement-related genes induced by PAX2 in renal tubules.

Xiu-Li Wang, Ling Hou, Cheng-Guang Zhao, Ying Tang, Bo Zhang, Jing-Ying Zhao, Yu-Bin Wu

Open access · hybridAbstract read
In one paragraph

Article in Nephrology (Carlton, Vic.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 32% of its field
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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Nicotinamide Attenuates Complement and Coagulation Pathways and Resultant Renal Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  3. Article
  4. Article
  5. Article
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

7 authors at 1 institution in 1 country.

Xiu-Li WangDepartment of Pediatric Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.
Ling HouDepartment of Pediatric Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.
Cheng-Guang ZhaoDepartment of Pediatric Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.
Ying TangDepartment of Pediatric Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.
Bo ZhangDepartment of Pediatric Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.
Jing-Ying ZhaoDepartment of Pediatric Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.
Yu-Bin WuDepartment of Pediatric Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.
China Medical University · CN

Funding

Science Plan Program of Liaoning Province, China 2013021099
6 · The paper itself

Abstract

aimThe aim of the present study was to screen and verify downstream genes involved in the epithelial mesenchymal transition (EMT) induced by paired box 2 (PAX2) in NRK-52E cells.

methodsNRK-52E cells were transfected with lentivirus carrying PAX2 gene or no-load virus respectively. Total RNA was isolated 72 h after transfection from PAX2-overexpressing cells and control cells. Isolated RNA was then hybridized with the Rat OneArray Plus expression profile chip. The chips were examined by Agilent 0.1 XDR to screen for differentially expressed genes, which were further analyzed to investigate complement-related genes as genes of interest.

resultsIn NRK-52E cells, PAX2 overexpression promoted EMT followed by upregulation of 298 genes and downregulation of 293 genes. KEGG analysis indicated the differential expression of genes related to cytokines and their receptors, extracellular matrix (ECM), MAPKs, local adhesion, cancer, the complement cascade, and coagulation. Gene oncology analysis screened out genes related to molecular functions (e.g., hydrolase activity, phospholipase activity, components of the ECM) and biological processes (e.g., cell development, signal transduction, phylogeny), and cell components (e.g., cytoplasm, cell membrane, and ECM). Analysis of the complement system revealed upregulation of C3 and downregulation of CD55 and complement regulator factor H (CFH).

conclusionPAX2 overexpression upregulates EMT in vitro and may regulate C3, CD55, and CFH.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsBlotting, WesternCD55 AntigensCell LineComplement C3Complement Factor HComplement System ProteinsGene Expression ProfilingGene Expression RegulationKidney TubulesOligonucleotide Array Sequence AnalysisPAX2 Transcription FactorRatsReal-Time Polymerase Chain ReactionSignal TransductionCD55 AntigensComplement C3Complement Factor HComplement System ProteinsPAX2 protein, ratPAX2 Transcription Factorcomplement genesepithelial-mesenchymal cell transitiongene ontologyKyoto Encyclopedia of Genes and GenomesNRK-52E cellsPaired box 2

Identifiers

PMID29280536
PMCPMC6585862
OpenAlexW2779919801

What OpenQuestion holds

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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.