Evidence map›Paper›PMID 10457094›Full record

ArticleThe Journal of physiology1999

Actin polymerization stimulated by contractile activation regulates force development in canine tracheal smooth muscle.

D Mehta, S J Gunst

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

88 citing papers in PubMed, 240 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  6. Review
  7. Dynamic cytosolic CaAmerican journal of physiology. Lung cellular and molecular physiology · 2021
    Article
  8. Mfge8 attenuates human gastric antrum smooth muscle contractions.Journal of muscle research and cell motility · 2021
    Article
  9. Article
  10. The wHole Story About Fenestrations in LSEC.Frontiers in physiology · 2021
    Review
  11. Effects of TNFα on Dynamic Cytosolic CaFrontiers in physiology · 2021
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Molecular Mechanisms for the Mechanical Modulation of Airway Responsiveness.Journal of engineering and science in medical diagnostics and therapy · 2019
    Article
  17. Article
  18. Article
  19. Actin polymerization contributes to enhanced pulmonary vasoconstrictor reactivity after chronic hypoxia.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  20. Elastase alters contractility and promotes an inflammatory synthetic phenotype in airway smooth muscle tissues.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article

28 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

D MehtaDepartment of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
S J Gunst
Indiana University School of Medicine

Funding

Smooth Muscle Mechanisms in Dynamic Airways PropertiesR01HL029289 · NHLBI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI GUNST, SUSAN J. · 1986 to 2020
$7.3M
SMOOTH MUSCLE MECHANISMS IN DYNAMIC AIRWAY PROPERTIESR23HL029289 · NHLBI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI GUNST, SUSAN J. · 1985 to 1985
–
NHLBI NIH HHS HL29289NHLBI NIH HHS R01 HL029289
6 · The paper itself

Abstract

1. The role of actin polymerization in the regulation of smooth muscle contractility was investigated in canine trachealis muscle strips. The effect of contractile activation on the content of monomeric globular (G)-actin was estimated by the method of DNase I inhibition. The G-actin content was 30 % lower in extracts of muscle strips activated with 10-4 M acetylcholine (ACh) than in extracts from unstimulated muscle strips. The decrease in G-actin in response to contractile stimulation was prevented by latrunculin-A, an agent that prevents actin polymerization by binding to G-actin monomers. 2. The inhibition of actin polymerization by latrunculin-A markedly depressed force development in response to ACh but had no effect on ACh-induced myosin light chain (MLC) phosphorylation. Latrunculin also suppressed the length sensitivity of force during ACh-induced isometric contractions. The actin-capping agent cytochalasin-D also markedly inhibited force and caused only a slight decrease in MLC phosphorylation. Cytochalasin-D also inhibited force in alpha-toxin-permeabilized muscle strips that were activated either by Ca2+ or by ACh at constant pCa. No disorganization of smooth muscle cell ultrastructure was detected by electron microscopy or by immunofluorescence microscopy of muscles treated with either agent. 3. The results suggest that the polymerization of actin is stimulated by the contractile activation of tracheal smooth muscle and that this actin polymerization contributes directly to force development. In addition, actin filament remodelling contributes to the length sensitivity of tracheal smooth muscle contractility.

Indexed as

Muscle ContractionAcetylcholineActinsAnimalsBridged Bicyclo Compounds, HeterocyclicCytochalasin DDogsMuscle, SmoothMyosin Light ChainsPhosphorylationPolymersThiazolesThiazolidinesTracheaAcetylcholineActinsBridged Bicyclo Compounds, HeterocyclicCytochalasin Dlatrunculin AMyosin Light ChainsPolymersThiazolesThiazolidines

Identifiers

PMID10457094
PMCPMC2269534
OpenAlexW2037425060

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.