Evidence map›Paper›PMID 32658594›Full record

ArticleCell cycle (Georgetown, Tex.)2020

SCF/c-kit signaling pathway participates in ICC damage in neurogenic bladder.

Yuan Ma, Yan Chen, Yan Zheng, Yibo Wen, Yunlong Li, Jinjin Feng, Yulin He, Jianguo Wen

Open access · bronzeAbstract read
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2020. 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
1.3field-weighted citation impact, top 20% 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, 13 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Yuan MaInstitute of Clinical Medicine, Urodynamic Center and Department of Urology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Yan ChenInstitute of Clinical Medicine, Urodynamic Center and Department of Urology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Yan ZhengImmunization Key Lab of Kidney Disease of Henan Province, People's Hospital of Henan Province, Zhengzhou University , Zhengzhou, China.
Yibo WenDepartment of Urology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Yunlong LiDepartment of Urology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Jinjin FengDepartment of Urology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Yulin HeDepartment of Urology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
Jianguo WenInstitute of Clinical Medicine, Urodynamic Center and Department of Urology, Institute of Clinical Medicine, Pediatric Urodynamic Center and Department of Urology, The First Affiliated Hospital of Zhengzhou University , Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CNZhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurogenic bladder (NB) is a type of double renal dysfunction caused by nerve lesions. The interstitial cells of Cajal (ICC) damage are involved in bladder dysfunction. The aim of this study is to investigate the effect of stem cell factor (SCF)/c-kit signaling pathway on ICC damage in NB model rats. Maximum cystometric capacity (MCC), bladder leak point pressures (BLPP), and bladder compliance (BC) were measured in sham-operated and NB model rats. Immunofluorescent staining for c-kit was performed to determine ICC count in rat bladder trigone. The morphology and ultrastructure changes of ICCs were observed under an electron microscope. The mRNA levels of c-kit and SCF in bladder tissues were determined by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The protein levels of c-kit, SCF, p-JAK, p-STAT1, and p-STAT3 in bladder tissues were determined by western blot. ICC proliferation was detected by CCK-8 assay. NB resulted in changes in ultrastructure changes of ICCs and a decrease in the number of ICCs and in expression of c-kit, SCF, p-JAK, p-STAT1, and p-STAT3 in NB tissues. Inhibition of SCF/c-kit signaling pathway suppressed ICC proliferation by inhibiting JAK/STAT3 pathway. Moreover, inhibition of SCF/c-kit signaling pathway impaired the SCF-induced attenuation of ICC damage in NB model rats. Collectively, our data indicate that SCF/c-kit signaling pathway participates in ICC damage in NB.

Indexed as

AnimalsCell CountCell ProliferationDisease Models, AnimalFemaleInterstitial Cells of CajalJanus KinasesProto-Oncogene Proteins c-kitRats, Sprague-DawleySignal TransductionSTAT Transcription FactorsStem Cell FactorUrinary Bladder, NeurogenicJanus KinasesProto-Oncogene Proteins c-kitSTAT Transcription FactorsStem Cell Factorinterstitial cells of Cajalneurogenic bladderStem cell factor/c-kit

Identifiers

PMID32658594
PMCPMC7469680
OpenAlexW3043672405

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.