Evidence map›Paper›PMID 21131638›Full record

ArticleCardiovascular research2011

Rac1 and RhoA differentially regulate angiotensinogen gene expression in stretched cardiac fibroblasts.

Suresh K Verma, Hind Lal, Honey B Golden, Fnu Gerilechaogetu, Manuela Smith, Rakeshwar S Guleria, Donald M Foster, Guangrong Lu, David E Dostal

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2011. 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
3.4field-weighted citation impact, top 7% 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, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Targeting the renin-angiotensin-aldosterone system in fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Critical effects of long non-coding RNA on fibrosis diseases.Experimental & molecular medicine · 2018
    Review
  14. Article
  15. Article
  16. New Treatment Strategies for Alcohol-Induced Heart Damage.International journal of molecular sciences · 2016
    Review
  17. Noncoding RNA as regulators of cardiac fibrosis: current insight and the road ahead.Pflugers Archiv : European journal of physiology · 2016
    Review
  18. Integrins and integrin-related proteins in cardiac fibrosis.Journal of molecular and cellular cardiology · 2016
    Review
  19. Review
  20. Interleukin-10 inhibits chronic angiotensin II-induced pathological autophagy.Journal of molecular and cellular cardiology · 2015
    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

9 authors at 5 institutions in 1 country.

Suresh K VermaFeinberg Cardiovascular Research Institute, Northwestern University, Chicago, IL, USA.
Hind Lal
Honey B Golden
Fnu Gerilechaogetu
Manuela Smith
Rakeshwar S Guleria
Donald M Foster
Guangrong Lu
David E Dostal
Texas A&M Health Science Center · USCentral Texas Veterans Health Care System · USNorthwestern University · USTexas A&M Health Science Center · USThomas Jefferson University · US

Funding

Mechanical Signaling Mechanisms in Cardiac TissueR01HL068838 · NHLBI · TEXAS A&M UNIVERSITY HEALTH SCIENCE CTR · PI DOSTAL, DAVID E · 2004 to 2013
$2.3M
NHLBI NIH HHS 5R01-HL068838-6NHLBI NIH HHS R01 HL068838
6 · The paper itself

Abstract

aimsAngiotensin II (Ang II) stimulates cardiac remodelling and fibrosis in the mechanically overloaded myocardium. Although Rho GTPases regulate several cellular processes, including myocardial remodelling, involvement in mediating mechanical stretch-induced regulation of angiotensinogen (Ao), the precursor to Ang II, remains to be determined. We, therefore, examined the role and associated signalling mechanisms of Rho GTPases (Rac1 and RhoA) in regulation of Ao gene expression in a stretch model of neonatal rat cardiac fibroblasts (CFs). METHODS AND

resultsCFs were plated on deformable stretch membranes. Equiaxial mechanical stretch caused significant activation of both Rac1 and RhoA within 2-5 min. Rac1 activity returned to control levels after 4 h, whereas RhoA remained at a high level of activity until the end of the stretch period (24 h). Mechanical stretch initially caused a moderate decrease in Ao gene expression, but was significantly increased at 8-24 h. RhoA had a major role in mediating both the stretch-induced inhibition of Ao at 4 h and the subsequent upregulation of Ao expression at 24 h. β₁ integrin receptor blockade by Tac β₁ expression impaired acute (2 and 15 min) stretch-induced Rac1 activation, but increased RhoA activity. Molecular experiments revealed that Ao gene expression was inhibited by Rac1 through both JNK-dependent and independent mechanisms, and stimulated by RhoA through a p38-dependent mechanism.

conclusionThese results indicate that stretch-induced activation of Rac1 and RhoA differentially regulates Ao gene expression by modulating p38 and JNK activation.

Indexed as

Cell ShapeMechanotransduction, CellularAngiotensinogenAnimalsAnimals, NewbornCells, CulturedEnzyme ActivationFibroblastsGene Expression RegulationIntegrin beta1JNK Mitogen-Activated Protein KinasesMyocardiump38 Mitogen-Activated Protein KinasesPhosphorylationrac1 GTP-Binding ProteinRatsAngiotensinogenIntegrin beta1JNK Mitogen-Activated Protein Kinasesp38 Mitogen-Activated Protein Kinasesrac1 GTP-Binding ProteinRac1 protein, ratRecombinant Fusion ProteinsrhoA GTP-Binding Protein

Identifiers

PMID21131638
PMCPMC3058736
OpenAlexW2112707577

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.