Evidence map›Paper›PMID 24393526›Full record

ArticleBMB reports2014

Type 3 muscarinic acetylcholine receptor stimulation is a determinant of endothelial barrier function and adherens junctions integrity: role of protein-tyrosine phosphatase 1B.

Zhou-Yang Jiao, Jing Wu, Chao Liu, Bing Wen, Wen-Zeng Zhao, Xin-Ling Du

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMB reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.1field-weighted citation impact, top 46% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. The Role of Muscarinic Acetylcholine Receptor MInternational journal of molecular sciences · 2024
    Review
  3. Review
  4. Topical Donepezil for Cholinergic Modulation in Chronic Wound Repair.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
    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

6 authors at 1 institution in 1 country.

Zhou-Yang JiaoDepartment of Cardiovascular Surgery, Xiehe Hospital, Huazhong University of Science and Technology, Wuhan 430022; Department of Cardiovascular Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Jing WuDepartment of Pediatrics, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Chao LiuDepartment of Cardiovascular Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Bing WenDepartment of Cardiovascular Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Wen-Zeng ZhaoDepartment of Cardiovascular Surgery, First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Xin-Ling DuDepartment of Cardiovascular Surgery, Xiehe Hospital, Huazhong University of Science and Technology, Wuhan 430022, China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The main purpose of this study was to investigate whether type 3 muscarinic acetylcholine receptor (M3R) dysfunction induced vascular hyperpermeability. Transwell system analysis showed that M3R inhibition by selective antagonist 4-diphenylacetoxy-N-methylpiperidine methiodide (4-DAMP) and small interfering RNA both increased endothelial permeability. Using coimmunoprecipitation and Western blot assay, we found that M3R inhibition increased VE-cadherin and β-catenin tyrosine phosphorylation without affecting their expression. Using PTP1B siRNA, we found that PTP1B was required for maintaining VE-cadherin and β-catenin protein dephosphorylation. In addition, 4-DAMP suppressed PTP1B activity by reducing cyclic adenosine monophosphate (cAMP), but not protein kinase Cα (PKCα). These data indicate that M3R preserves the endothelial barrier function through a mechanism potentially maintaining PTP1B activity, keeping the adherens junction proteins (AJPs) dephosphorylation.

Indexed as

Adherens JunctionsAntigens, CDbeta CateninCadherin 5CadherinsCell Membrane PermeabilityCyclic AMPEndothelium, VascularHumansHuman Umbilical Vein Endothelial CellsPhosphorylationPhosphotyrosineProtein Kinase C-alphaProtein Tyrosine Phosphatase, Non-Receptor Type 1Receptor, Muscarinic M3Receptors, MuscarinicAntigens, CDbeta CateninCadherin 5CadherinsCHRM3 protein, humanCyclic AMPPhosphotyrosineProtein Kinase C-alphaProtein Tyrosine Phosphatase, Non-Receptor Type 1PTPN1 protein, humanReceptor, Muscarinic M3Receptors, Muscarinic

Identifiers

PMID24393526
PMCPMC4261512
OpenAlexW2051870955

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.