Evidence map›Paper›PMID 10079099›Full record

ArticleThe Journal of clinical investigation1999

Agonist-stimulated cytoskeletal reorganization and signal transduction at focal adhesions in vascular smooth muscle cells require c-Src.

T Ishida, M Ishida, J Suero, M Takahashi, B C Berk

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.6field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 159 citations in OpenAlex.

  1. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  2. The role of tensins in malignant neoplasms.Archives of medical science : AMS · 2023
    Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Integrin signaling in atherosclerosis.Cellular and molecular life sciences : CMLS · 2017
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Increased vascular smooth muscle cell stiffness: a novel mechanism for aortic stiffness in hypertension.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  17. Article
  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

5 authors at 3 institutions in 2 countries.

T IshidaDepartment of Medicine, Cardiology Division, University of Washington School of Medicine, Seattle, Washington 98195, USA. tishida@mcai.med.hiroshima-u.ac.jp
M Ishida
J Suero
M Takahashi
B C Berk
University of Washington · USHiroshima University · JPUniversity of Rochester · US

Funding

Regulation of Na+/H+ Exchange Vascular Smooth MuscleR01HL044721 · NHLBI · UNIVERSITY OF WASHINGTON · PI BERK, BRADFORD C · 1991 to 2004
$1.3M
MAP KINASE PHOSPHATASE (MKP 1) AND SMOOTH MUSCLE GROWTHF32HL009372 · NHLBI · UNIVERSITY OF WASHINGTON · PI SUERO, JAMES A · 1995 to 1996
–
NHLBI NIH HHS F32 HL009372NHLBI NIH HHS HL-09372NHLBI NIH HHS HL-44721NHLBI NIH HHS R01 HL044721
6 · The paper itself

Abstract

Thrombin and angiotensin II (angII) have trophic properties as mediators of vascular remodeling. Focal adhesions and actin cytoskeleton are involved in cell growth, shape, and movement and may be important in vascular remodeling. To characterize mechanisms by which thrombin and angII modulate vessel structure, we studied the effects of these G protein-coupled receptor ligands on focal adhesions in vascular smooth muscle cells (VSMCs). Both thrombin and angII stimulated bundling of actin filaments to form stress fibers, assembly of focal adhesions, and protein tyrosine phosphorylation at focal adhesions, such as p130Cas, paxillin, and tensin. To test whether c-Src plays a critical role in focal adhesion rearrangement, we analyzed cells with altered c-Src activity by retroviral transduction of wild-type (WT) and kinase-inactive (KI) c-Src into rat VSMCs, and by use of VSMCs from WT (src+/+) and Src-deficient (src-/-) mice. Tyrosine phosphorylation of Cas, paxillin, and tensin were markedly decreased in VSMCs expressing KI-Src and in src-/- VSMCs. Expression of KI-Src did not inhibit stress fiber formation by thrombin. Surprisingly, actin bundling was markedly decreased in VSMCs from src-/- mice both basally and after thrombin stimulation, compared with src+/+ mice. We also studied the effect of KI-Src and WT-Src on VSMC spreading. Expression of KI-Src reduced the rate of VSMC spreading on collagen, whereas WT-Src enhanced cell spreading. In conclusion, c-Src plays a critical role in agonist-stimulated cytoskeletal reorganization and signal transduction at focal adhesions in VSMCs. c-Src kinase activity is required for the cytoskeletal turnover that occurs in cell spreading, whereas c-Src appears to regulate actin bundling via a kinase-independent mechanism.

Indexed as

ProteinsAngiotensin IIAnimalsAortaBiological TransportCell AdhesionCell CompartmentationCrk-Associated Substrate ProteinCytoskeletal ProteinsCytoskeletonIntercellular JunctionsMiceMicrofilament ProteinsMuscle, Smooth, VascularMutationPaxillinAngiotensin IIBcar1 protein, mouseBcar1 protein, ratCrk-Associated Substrate ProteinCytoskeletal ProteinsMicrofilament ProteinsPaxillinPhosphoproteinsProteinsProto-Oncogene Proteins pp60(c-src)Pxn protein, mousePxn protein, ratRetinoblastoma-Like Protein p130TensinsThrombinTns1 protein, rat

Identifiers

PMID10079099
PMCPMC408136
OpenAlexW2007349364

What OpenQuestion holds

Texttitle and abstract
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.