Evidence map›Paper›PMID 23499953›Full record

ArticleGastroenterology2013

Altered contractile phenotypes of intestinal smooth muscle in mice deficient in myosin phosphatase target subunit 1.

Wei-Qi He, Yan-Ning Qiao, Ya-Jing Peng, Juan-Min Zha, Cheng-Hai Zhang, Chen Chen, Cai-Ping Chen, Pei Wang, Xiao Yang, Chao-Jun Li and 3 more

Open access · greenAbstract read
In one paragraph

Article in Gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

47 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. MBNL loss of function in smooth muscle as a model for myotonic dystrophy associated gastrointestinal dysmotility.Proceedings of the National Academy of Sciences of the United States of America · 2025
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  6. MYPT1Translational stroke research · 2024
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  11. Regulation of myosin light-chain phosphorylation and its roles in cardiovascular physiology and pathophysiology.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Review
  12. Article
  13. Mfge8 attenuates human gastric antrum smooth muscle contractions.Journal of muscle research and cell motility · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 6 institutions in 2 countries.

Wei-Qi HeModel Animal Research Center and MOE Key Laboratory of Model Animal for Disease Study, Nanjing University, Nanjing, China.
Yan-Ning Qiao
Ya-Jing Peng
Juan-Min Zha
Cheng-Hai Zhang
Chen Chen
Cai-Ping Chen
Pei Wang
Xiao Yang
Chao-Jun Li
Kristine E Kamm
James T Stull
Min-Sheng Zhu
Model Animal Research Center · CNNanjing University · CNThe University of Texas Southwestern Medical Center · USNanjing Medical University · CNState Key Laboratory of ProteomicsWenzhou Medical University · CN

Funding

MYOSIN LIGHT CHAIN KINASE FUNCTION IN SMOOTH MUSCLER01HL026043 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI STULL, JAMES T · 1985 to 2009
$3.4M
Signal transduction mechanisms to myosin phosphataseR01HL112778 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI STULL, JAMES T · 2013 to 2016
$1.6M
NHLBI NIH HHS R01 HL026043NHLBI NIH HHS R01HL026043NHLBI NIH HHS R01 HL112778
6 · The paper itself

Abstract

BACKGROUND &

aimsThe regulatory subunit of myosin light chain phosphatase, MYPT1, has been proposed to control smooth muscle contractility by regulating phosphorylation of the Ca(2+)-dependent myosin regulatory light chain. We generated mice with a smooth muscle-specific deletion of MYPT1 to investigate its physiologic role in intestinal smooth muscle contraction.

methodsWe used the Cre-loxP system to establish Mypt1-floxed mice, with the promoter region and exon 1 of Mypt1 flanked by 2 loxP sites. These mice were crossed with SMA-Cre transgenic mice to generate mice with smooth muscle-specific deletion of MYPT1 (Mypt1(SMKO) mice). The phenotype was assessed by histologic, biochemical, molecular, and physiologic analyses.

resultsYoung adult Mypt1(SMKO) mice had normal intestinal motility in vivo, with no histologic abnormalities. On stimulation with KCl or acetylcholine, intestinal smooth muscles isolated from Mypt1(SMKO) mice produced robust and increased sustained force due to increased phosphorylation of the myosin regulatory light chain compared with muscle from control mice. Additional analyses of contractile properties showed reduced rates of force development and relaxation, and decreased shortening velocity, compared with muscle from control mice. Permeable smooth muscle fibers from Mypt1(SMKO) mice had increased sensitivity and contraction in response to Ca(2+).

conclusionsMYPT1 is not essential for smooth muscle function in mice but regulates the Ca(2+) sensitivity of force development and contributes to intestinal phasic contractile phenotype. Altered contractile responses in isolated tissues could be compensated by adaptive physiologic responses in vivo, where gut motility is affected by lower intensities of smooth muscle stimulation for myosin phosphorylation and force development.

Indexed as

AnimalsCalciumCalcium SignalingFemaleGastrointestinal MotilityIntestinesMaleMiceMice, KnockoutMuscle ContractionMuscle, SmoothMyosin-Light-Chain KinaseMyosin-Light-Chain PhosphataseCalciumMyosin-Light-Chain KinaseMyosin-Light-Chain PhosphatasePpp1r12a protein, mouse

Identifiers

PMID23499953
PMCPMC3782749
OpenAlexW1974033740

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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.