Evidence map›Paper›PMID 28806761›Full record

ArticlePloS one2017

Transcriptome analysis of PDGFRα+ cells identifies T-type Ca2+ channel CACNA1G as a new pathological marker for PDGFRα+ cell hyperplasia.

Se Eun Ha, Moon Young Lee, Masaaki Kurahashi, Lai Wei, Brian G Jorgensen, Chanjae Park, Paul J Park, Doug Redelman, Kent C Sasse, Laren S Becker and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Roles of PDGF/PDGFR signaling in various organs.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
    Review
  4. Article
  5. Article
  6. Blockade of CaBritish journal of pharmacology · 2024
    Article
  7. Article
  8. Interstitial cells of the sip syncytium regulate basal membrane potential in murine gastric corpus.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  9. Article
  10. CaPhysiological reviews · 2024
    Review
  11. Article
  12. Article
  13. The enteric nervous system.Physiological reviews · 2023
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. CaAdvances in experimental medicine and biology · 2022
    Article
  19. Article
  20. 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

12 authors at 2 institutions in 2 countries.

Se Eun HaDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada, United States of America.
Moon Young LeeDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada, United States of America.
Masaaki KurahashiDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada, United States of America.
Lai WeiDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada, United States of America.
Brian G JorgensenDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada, United States of America.
Chanjae ParkDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada, United States of America.
Paul J ParkDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada, United States of America.
Doug RedelmanDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada, United States of America.
Kent C SasseSasse Surgical Associates, Reno, Nevada, United States of America.
Laren S BeckerGastroenterology and Hepatology, Stanford University School of Medicine, Stanford, California, United States of America.
Kenton M SandersDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada, United States of America.
Seungil RoDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, Nevada, United States of America.ORCID http://orcid.org/0000-0003-0861-8334
University of Nevada, Reno · USStanford University · US

Funding

Tissue, Cell and Tissue Culture CoreP01DK041315 · NIDDK · UNIVERSITY OF NEVADA RENO · PI KEEF, KATHLEEN D · 1989 to 2018
$26.3M
Inhibitory mechanisms of PDGFRa+ interstitial cells in gastrointestinal motilityR01DK091336 · NIDDK · UNIVERSITY OF NEVADA RENO · PI KURAHASHI, MASAAKI · 2013 to 2022
$4.3M
Roles of DNA methylation in gastrointestinal smooth muscle cellsR01DK094886 · NIDDK · UNIVERSITY OF NEVADA RENO · PI RO, SEUNGIL · 2012 to 2016
$1.5M
Engineering of functional smooth muscle cells from gastrointestinal myofibroblastR01DK103055 · NIDDK · UNIVERSITY OF NEVADA RENO · PI RO, SEUNGIL · 2015 to 2018
$1.3M
NIDDK NIH HHS P01 DK041315NIDDK NIH HHS R01 DK091336NIDDK NIH HHS R01 DK094886NIDDK NIH HHS R01 DK103055
6 · The paper itself

Abstract

Platelet-derived growth factor receptor alpha (PDGFRα)+ cells are distributed into distinct morphological groups within the serosal, muscular, and submucosal layers as well as the myenteric and deep muscular plexi. PDGFRα+ cells directly interact with interstitial cells of Cajal (ICC) and smooth muscle cells (SMC) in gastrointestinal smooth muscle tissue. These three cell types, SMC, ICC, and PDGFRα+ cells (SIP cells), form an electrical syncytium, which dynamically regulates gastrointestinal motility. We have previously reported the transcriptomes of SMC and ICC. To complete the SIP cell transcriptome project, we obtained transcriptome data from jejunal and colonic PDGFRα+ cells. The PDGFRα+ cell transcriptome data were added to the Smooth Muscle Genome Browser that we previously built for the genome-scale gene expression data of ICC and SMC. This browser provides a comprehensive reference for all transcripts expressed in SIP cells. By analyzing the transcriptomes, we have identified a unique set of PDGFRα+ cell signature genes, growth factors, transcription factors, epigenetic enzymes/regulators, receptors, protein kinases/phosphatases, and ion channels/transporters. We demonstrated that the low voltage-dependent T-type Ca2+ channel Cacna1g gene was particularly expressed in PDGFRα+ cells in the intestinal serosal layer in mice. Expression of this gene was significantly induced in the hyperplasic PDGFRα+ cells of obstructed small intestine in mice. This gene was also over-expressed in colorectal cancer, Crohn's disease, and diverticulitis in human patients. Taken together, our data suggest that Cacna1g exclusively expressed in serosal PDGFRα+ cells is a new pathological marker for gastrointestinal diseases.

Indexed as

Gene Expression ProfilingAnimalsCalcium Channels, T-TypeCell DedifferentiationCell ProliferationCell SeparationGene Expression RegulationGenomeHumansHyperplasiaHypertrophyIon ChannelsJejunumMiceMuscle, SmoothProtein IsoformsCACNA1G protein, humanCacna1g protein, mouseCalcium Channels, T-TypeIon ChannelsProtein IsoformsReceptor, Platelet-Derived Growth Factor alphaRNA, Messenger

Identifiers

PMID28806761
PMCPMC5555714
OpenAlexW2749335473

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.