Evidence map›Paper›PMID 24914207›Full record

ArticleThe Journal of biological chemistry2014

Cytoskeletal reorganization evoked by Rho-associated kinase- and protein kinase C-catalyzed phosphorylation of cofilin and heat shock protein 27, respectively, contributes to myogenic constriction of rat cerebral arteries.

Alejandro Moreno-Domínguez, Ahmed F El-Yazbi, Hai-Lei Zhu, Olaia Colinas, X Zoë Zhong, Emma J Walsh, Dylan M Cole, Gary J Kargacin, Michael P Walsh, William C Cole

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Heat Shock Proteins in Tooth Development and Injury Repair.International journal of molecular sciences · 2023
    Review
  9. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. EPAC in Vascular Smooth Muscle Cells.International journal of molecular sciences · 2020
    Review
  18. Article
  19. Article
  20. 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

10 authors at 2 institutions in 1 country.

Alejandro Moreno-Domínguez
Ahmed F El-Yazbi
Hai-Lei Zhu
Olaia Colinas
X Zoë Zhong
Emma J Walsh
Dylan M Cole
Gary J Kargacin
Michael P Walsh
William C Cole
Libin Cardiovascular Institute of Alberta · CAUniversity of Calgary · CA

Funding

Canadian Institutes of Health Research MOP-13505Canadian Institutes of Health Research MOP-97988
6 · The paper itself

Abstract

Our understanding of the molecular events contributing to myogenic control of diameter in cerebral resistance arteries in response to changes in intravascular pressure, a fundamental mechanism regulating blood flow to the brain, is incomplete. Myosin light chain kinase and phosphatase activities are known to be increased and decreased, respectively, to augment phosphorylation of the 20-kDa regulatory light chain subunits (LC20) of myosin II, which permits cross-bridge cycling and force development. Here, we assessed the contribution of dynamic reorganization of the actin cytoskeleton and thin filament regulation to the myogenic response and serotonin-evoked constriction of pressurized rat middle cerebral arteries. Arterial diameter and the levels of phosphorylated LC(20), calponin, caldesmon, cofilin, and HSP27, as well as G-actin content, were determined. A decline in G-actin content was observed following pressurization from 10 mm Hg to between 40 and 120 mm Hg and in three conditions in which myogenic or agonist-evoked constriction occurred in the absence of a detectable change in LC20 phosphorylation. No changes in thin filament protein phosphorylation were evident. Pressurization reduced G-actin content and elevated the levels of cofilin and HSP27 phosphorylation. Inhibitors of Rho-associated kinase and PKC prevented the decline in G-actin; reduced cofilin and HSP27 phosphoprotein content, respectively; and blocked the myogenic response. Furthermore, phosphorylation modulators of HSP27 and cofilin induced significant changes in arterial diameter and G-actin content of myogenically active arteries. Taken together, our findings suggest that dynamic reorganization of the cytoskeleton involving increased actin polymerization in response to Rho-associated kinase and PKC signaling contributes significantly to force generation in myogenic constriction of cerebral resistance arteries.

Indexed as

Actin CytoskeletonActin Depolymerizing FactorsAnimalsCalcium-Binding ProteinsCalponinsCerebral Arterial DiseasesConstriction, PathologicG-Protein-Coupled Receptor Kinase 1HSP27 Heat-Shock ProteinsMicrofilament ProteinsMiddle Cerebral ArteryPhosphorylationProtein Kinase CRatsRats, Sprague-DawleyActin Depolymerizing FactorsCalcium-Binding ProteinsCalponinsG-Protein-Coupled Receptor Kinase 1Grk1 protein, ratHSP27 Heat-Shock ProteinsHspb1 protein, ratMicrofilament ProteinsProtein Kinase C

Identifiers

PMID24914207
PMCPMC4110300
OpenAlexW2047729770

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.