Evidence map›Paper›PMID 39689119›Full record

ArticlePloS one2024

Colonic dysmotility regulated by downregulation of PDGFRα+ cells / SK3 channel in DSS-induced colitis mice.

Chen Lu, Hongxia Zhu, Haiqian Lu, Xianjing Xie, Ling Tong, Yujia Li, Zhida Qian

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Small-Conductance CaNeuroscience bulletin · 2026
    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

7 authors.

Chen LuThe International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Hongxia ZhuThe International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Haiqian LuThe International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Xianjing XieThe International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Ling TongDepartment of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yujia LiDepartment of Anatomy and Physiology, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Zhida QianThe International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.ORCID 0000-0001-8020-0501

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Colitis is a complex multifactorial disease with an unknown aetiology that mainly manifests as chronic refractory colon transmission disorders. Smooth muscle, the main source of colon transmission power, consists of not only smooth muscle cells (SMCs) but also PDGFRα+ cells that mediate smooth muscle relaxation and ICCs that mediate contraction. PDGFRα+ cells and their unique small conductance Ca2+-activated K (SK3) channels are crucial in regulating colonic transit by exerting inhibitory effects. In this study, the contributions of the SK3 signalling pathway in PDGFRα+ cells to colitis-induced colonic transit dysmotility were investigated in DSS-induced colitis mice. An experiment was conducted to record the transmission of waves during smooth muscle contraction in the colon, using a colonic migrating motor complex(CMMC). Western blotting was utilized for protein expression detection, while PCR was employed for gene expression analysis. Immunofluorescence staining was used to detect the co-localization of SK3 channels with PDGFRα+ cells. In the colitis group, the weight of mice was reduced, the length of colon was shortened, and the disease activity index (DAI) was significantly increased. In the CMMC experiment, colon transmission was significantly disrupted in the colitis group compared to the control group, with a consistent colonic transmission amplitude and frequency. The sensitivity of mice with colitis to SK3 antagonists and agonists (apamin and CyPPA) was lower than that of the control group in CMMC experiment. The expression levels of mRNA and protein of PDGFRα and SK3 channels in colon of mice with colitis were decreased. Less SK3 channel colocalization with PDGFRα+ cells was observed in the colitis mouse group than in the control group. The findings indicated that colonic transit disorder in DSS-induced colitis mice is caused by the down-regulation of PDGFRα+ cells / SK3 channel expression.

Indexed as

ColitisColonDextran SulfateDown-RegulationReceptor, Platelet-Derived Growth Factor alphaSmall-Conductance Calcium-Activated Potassium ChannelsAnimalsGastrointestinal MotilityMaleMiceMice, Inbred C57BLMuscle ContractionDextran SulfateKcnn3 protein, mouseReceptor, Platelet-Derived Growth Factor alphaSmall-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID39689119
PMCPMC11651619

What Socratic holds

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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.