Evidence map›Paper›PMID 33987885›Full record

ArticleCell proliferation2021

Activated mesangial cells induce glomerular endothelial cells proliferation in rat anti-Thy-1 nephritis through VEGFA/VEGFR2 and Angpt2/Tie2 pathway.

Yinghua Zhao, Bo Fu, Pu Chen, Qinggang Li, Qing Ouyang, Chuyue Zhang, Guangyan Cai, Lingling Wu, Xiangmei Chen

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 28 citations in OpenAlex.

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  8. Research (Washington, D.C.) · 2025
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  16. Article
  17. The Glomerulus According to the Mesangium.Frontiers in medicine · 2021
    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 at 1 institution in 1 country.

Yinghua ZhaoDepartment of Nephrology, First Medical Center of Chinese PLA General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.ORCID https://orcid.org/0000-0003-2101-392X
Bo FuDepartment of Nephrology, First Medical Center of Chinese PLA General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Pu ChenDepartment of Nephrology, First Medical Center of Chinese PLA General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Qinggang LiDepartment of Nephrology, First Medical Center of Chinese PLA General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Qing OuyangDepartment of Nephrology, First Medical Center of Chinese PLA General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Chuyue ZhangDepartment of Nephrology, First Medical Center of Chinese PLA General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Guangyan CaiDepartment of Nephrology, First Medical Center of Chinese PLA General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Lingling WuDepartment of Nephrology, First Medical Center of Chinese PLA General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Xiangmei ChenDepartment of Nephrology, First Medical Center of Chinese PLA General Hospital, Nephrology Institute of the Chinese People's Liberation Army, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases, Beijing Key Laboratory of Kidney Disease Research, Beijing, China.
Chinese PLA General Hospital · CN

Funding

National Natural Science Foundation of China 81330019National Natural Science Foundation of China 81830019National Natural Science Foundation of China 82070741PLA General Hospital Science and Technology Innovation Nursery Fund Project Nursery Fund Project 18KMM07Science and Technology Project of Beijing, China D181100000118002Science and Technology Project of Beijing, China D181100000118004Science and Technology Project of Beijing, China D181107000100000
6 · The paper itself

Abstract

objectivesWe aimed to investigate the underlying mechanism of endothelial cells (ECs) proliferation in anti-Thy-1 nephritis. MATERIALS AND

methodsWe established anti-Thy-1 nephritis and co-culture system to explore the underlying mechanism of ECs proliferation in vivo and in vitro. EdU assay kit was used for measuring cell proliferation. Immunohistochemical staining and immunofluorescence staining were used to detect protein expression. ELISA was used to measure the concentration of protein in serum and medium. RT-qPCR and Western blot were used to qualify the mRNA and protein expression. siRNA was used to knock down specific protein expression.

resultsIn anti-Thy-1 nephritis, ECs proliferation was associated with mesangial cells (MCs)-derived vascular endothelial growth factor A (VEGFA) and ECs-derived angiopoietin2 (Angpt2). In vitro co-culture system activated MCs-expressed VEGFA to promote vascular endothelial growth factor receptor2 (VEGFR2) activation, Angpt2 expression and ECs proliferation, but inhibit TEK tyrosine kinase (Tie2) phosphorylation. MCs-derived VEGFA stimulated Angpt2 expression in ECs, which inhibited Tie2 phosphorylation and promoted ECs proliferation. And decline of Tie2 phosphorylation induced ECs proliferation. In anti-Thy-1 nephritis, promoting Tie2 phosphorylation could alleviate ECs proliferation.

conclusionsOur study showed that activated MCs promoted ECs proliferation through VEGFA/VEGFR2 and Angpt2/Tie2 pathway in experimental mesangial proliferative glomerulonephritis (MPGN) and in vitro co-culture system. And enhancing Tie2 phosphorylation could alleviate ECs proliferation, which will provide a new idea for MPGN treatment.

Indexed as

Signal TransductionAngiopoietin-2AnimalsAntibodiesCell ProliferationDisease Models, AnimalEndothelial CellsGlomerulonephritisKidney GlomerulusMaleMesangial CellsRatsRats, WistarReceptor, TIE-2Thy-1 AntigensVascular Endothelial Growth Factor AAngiopoietin-2AntibodiesKdr protein, ratReceptor, TIE-2Thy-1 AntigensVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2Angpt2/Tie2 pathwayglomerular endothelial cellsmesangial cellsmesangial proliferative glomerulonephritisVEGFA/VEGFR2 pathway

Identifiers

PMID33987885
PMCPMC8168418
OpenAlexW3161227023

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.