Evidence map›Paper›PMID 21593453›Full record

ArticleAmerican journal of physiology. Cell physiology2011

PDGF-dependent regulation of regulator of G protein signaling-5 expression and vascular smooth muscle cell functionality.

Jagadambika J Gunaje, Arya J Bahrami, Stephen M Schwartz, Guenter Daum, William M Mahoney

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Molecular Regulation of the Response of Brain Pericytes to Hypoxia.International journal of molecular sciences · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The Ion Channel and GPCR Toolkit of Brain Capillary Pericytes.Frontiers in cellular neuroscience · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  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

5 authors at 1 institution in 1 country.

Jagadambika J GunajeDepartment of Pathology and Center for Cardiovascular Biology, University of Washington, Seattle, WA 98109, USA.
Arya J Bahrami
Stephen M Schwartz
Guenter Daum
William M Mahoney
University of Washington · US

Funding

EXPERIMENTAL PATHOLOGY OF CARDIOVASCULAR DISEASET32HL007312 · NHLBI · UNIVERSITY OF WASHINGTON · PI MAJESKY, MARK W., SCHWARTZ, STEPHEN MARK · 1985 to 2019
$11.8M
Molecular Characterization of Arterially-Restricted RGS5R00HL087513 · NHLBI · UNIVERSITY OF WASHINGTON · PI MAHONEY, WILLIAM M · 2009 to 2011
$747k
Molecular Characterization of Arterially-Restricted RGS5K99HL087513 · NHLBI · UNIVERSITY OF WASHINGTON · PI MAHONEY, WILLIAM M · 2007 to 2008
$160k
NHLBI NIH HHS HL-007312NHLBI NIH HHS HL-087513
6 · The paper itself

Abstract

Regulator of G protein signaling (RGS) proteins, and notably members of the RGS-R4 subfamily, control vasocontractility by accelerating the inactivation of Gα-dependent signaling. RGS5 is the most highly and differently expressed RGS-R4 subfamily member in arterial smooth muscle. Expression of RGS5 first appears in pericytes during development of the afferent vascular tree, suggesting that RGS5 is a good candidate for a regulator of arterial contractility and, perhaps, for determining the mass of the smooth muscle coats required to regulate blood flow in the branches of the arterial tree. Consistent with this hypothesis, using cultured vascular smooth muscle cells (VSMCs), we demonstrate RGS5 overexpression inhibits G protein-coupled receptor (GPCR)-mediated hypertrophic responses. The next objective was to determine which physiological agonists directly control RGS5 expression in VSMCs. GPCR agonists failed to directly regulate RGS5 mRNA expression; however, platelet-derived growth factor (PDGF) acutely represses expression. Downregulation of RGS5 results in the induction of migration and the activation of the GPCR-mediated signaling pathways. This stimulation leads to the activation of mitogen-activated protein kinases directly downstream of receptor stimulation, and ultimately VSMC hypertrophy. These results demonstrate that RGS5 expression is a critical mediator of both VSMC contraction and potentially, arterial remodeling.

Indexed as

Signal TransductionAngiotensin IIAnimalsBecaplerminCell LineCell MovementGene Expression RegulationHypertrophyLigandsMitogen-Activated Protein KinasesMuscle, Smooth, VascularMyocytes, Smooth MusclePlatelet-Derived Growth FactorProto-Oncogene Proteins c-sisRatsReceptors, G-Protein-CoupledAngiotensin IIBecaplerminLigandsMitogen-Activated Protein KinasesPlatelet-Derived Growth FactorProto-Oncogene Proteins c-sisReceptors, G-Protein-CoupledReceptors, Platelet-Derived Growth FactorRgs5 protein, ratRGS Proteins

Identifiers

PMID21593453
PMCPMC3154557
OpenAlexW2129333964

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.