Evidence map›Paper›PMID 15155793›Full record

ArticleThe Journal of physiology2004

Sequential activation of RhoA and FAK/paxillin leads to ATP release and actin reorganization in human endothelium.

Masakazu Hirakawa, Masahiro Oike, Yuji Karashima, Yushi Ito

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-weighted citation impact, top 17% 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

28 citing papers in PubMed, 66 citations in OpenAlex.

  1. Catalase-like activity of CoMikrochimica acta · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Paxillin: a crossroad in pathological cell migration.Journal of hematology & oncology · 2017
    Review
  9. Shear-Sensitive Genes in Aortic Valve Endothelium.Antioxidants & redox signaling · 2016
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Lysophosphatidic acid in atherosclerotic diseases.British journal of pharmacology · 2012
    Review
  15. Review
  16. Article
  17. Article
  18. 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

4 authors at 1 institution in 1 country.

Masakazu HirakawaDepartment of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan.
Masahiro Oike
Yuji Karashima
Yushi Ito
Kyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have investigated the cellular mechanisms of mechanical stress-induced immediate responses in human umbilical vein endothelial cells (HUVECs). Hypotonic stress (HTS) induced ATP release, which evoked a Ca(2+) transient, followed by actin reorganization within a few minutes, in HUVECs. Disruption of the actin cytoskeleton did not suppress HTS-induced ATP release, and inhibition of the ATP-mediated Ca(2+) response did not affect actin reorganization, thereby indicating that these two responses are not interrelated. ATP release and actin reorganization were also induced by lysophosphatidic acid (LPA). HTS and LPA induced membrane translocation of RhoA, which occurs when RhoA is activated, and tyrosine phosphorylation of focal adhesion kinase (FAK) and paxillin. Tyrosine kinase inhibitors (herbimycin A or tyrphostin 46) inhibited both HTS- and LPA-induced ATP release and actin reorganization, but did not affect RhoA activation. In contrast, Rho-kinase inhibitor (Y27632) inhibited all of the HTS- and LPA-induced responses. These results indicate that the activation of the RhoA/Rho-kinase pathway followed by tyrosine phosphorylation of FAK and paxillin leads to ATP release and actin reorganization in HUVECs. Furthermore, the fact that HTS and LPA evoke exactly the same intracellular signals and responses suggests that even these immediate mechanosensitive responses are in fact not mechanical stress-specific.

Indexed as

ActinsAdenosine TriphosphateCells, CulturedCytoskeletal ProteinsEndothelium, VascularEnzyme ActivatorsFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine KinasesHumansLysophospholipidsOsmotic PressurePaxillinPhosphoproteinsPhosphorylationProtein-Tyrosine KinasesrhoA GTP-Binding ProteinActinsAdenosine TriphosphateCytoskeletal ProteinsEnzyme ActivatorsFocal Adhesion Kinase 1Focal Adhesion Protein-Tyrosine Kinaseslysophosphatidic acidLysophospholipidsPaxillinPhosphoproteinsProtein-Tyrosine KinasesPTK2 protein, humanPXN protein, humanrhoA GTP-Binding ProteinTyrosine

Identifiers

PMID15155793
PMCPMC1664968
OpenAlexW1551940170

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.