Evidence map›Paper›PMID 22095985›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Regulation of peroxisome proliferator-activated receptor-γ by angiotensin II via transforming growth factor-β1-activated p38 mitogen-activated protein kinase in aortic smooth muscle cells.

Venkateswaran Subramanian, Jonathan Golledge, Elizabeth B Heywood, Dennis Bruemmer, Alan Daugherty

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Review
  6. Inducible Depletion of Calpain-2 Mitigates Abdominal Aortic Aneurysm in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2021
    Article
  7. Role of p38 MAPK in Atherosclerosis and Aortic Valve Sclerosis.International journal of molecular sciences · 2018
    Review
  8. Article
  9. NADPH oxidase 4 regulates vascular inflammation in aging and atherosclerosis.Journal of molecular and cellular cardiology · 2017
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Aortic aneurysms in Loeys-Dietz syndrome - a tale of two pathways?The Journal of clinical investigation · 2014
    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.

Venkateswaran SubramanianSaha Cardiovascular Research Center, BBSRB, Rm B249, University of Kentucky, Lexington, KY 40536-0509, USA. venkat.subramanian@uky.edu
Jonathan Golledge
Elizabeth B Heywood
Dennis Bruemmer
Alan Daugherty
James Cook University · AU

Funding

Specific Secretory Phospholipase A2 Isozymes Promote Aneurysm FormationP01HL080100 · NHLBI · UNIVERSITY OF KENTUCKY · PI MUKHERJEE, DEBABRATA · 2006 to 2010
$8.2M
Osteoprotegerin and osteopontin in aortic aneurysmR01HL080010 · NHLBI · JAMES COOK UNIVERSITY OF NO QUEENSLAND · PI GOLLEDGE, JONATHAN · 2005 to 2009
$1.3M
NHLBI NIH HHS HL80010NHLBI NIH HHS HL80100NHLBI NIH HHS P01 HL080100NHLBI NIH HHS R01 HL080010
6 · The paper itself

Abstract

objectivePeroxisome proliferator-activated receptor-γ (PPARγ) ligands attenuate angiotensin II (Ang II)-induced atherosclerosis through interactions with vascular smooth muscle cell (VSMC)-specific PPARγ in hypercholesterolemic mice. Therefore, the purpose of this study was to determine the mechanism of Ang II-mediated intracellular regulation of PPARγ in VSMCs. METHODS AND

resultsIncubation of cultured mouse aortic VSMCs with Ang II for 24 hours reduced abundance of PPARγ protein, mRNA, and transcriptional activity (P<0.001). This effect was attenuated by an angiotensin type 1 receptor antagonist, losartan. Ang II-induced PPARγ reduction was dependent on stimulation of transforming growth factor (TGF)-β1 as demonstrated using either a neutralizing antibody or small interfering RNA (siRNA). Ang II-induced TGF-β1 secretion was dependent on epidermal growth factor receptor kinase activation through reactive oxygen species production. Inhibition of p38 mitogen-activated protein kinase by SB203580 or siRNA inhibited both Ang II- and TGF-β1-induced PPARγ reduction. Blockade of TGF-β1 decreased p38 phosphorylation induced by Ang II. siRNA-mediated inhibition of histone deacetylase 3 attenuated p38-mediated reductions in PPARγ abundance.

conclusionsThese findings suggest that Ang II decreases PPARγ abundance in cultured VSMCs via an angiotensin type 1 receptor-dependent secretion of TGF-β1 via phosphorylation of p38 mitogen-activated protein kinase and histone deacetylase 3.

Indexed as

Angiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsAortaCells, CulturedEnzyme InhibitorsHistone Deacetylase 3Histone DeacetylasesImidazolesLosartanMaleMiceMice, Inbred C57BLModels, AnimalMuscle, Smooth, Vascularp38 Mitogen-Activated Protein KinasesAngiotensin IIAngiotensin II Type 1 Receptor BlockersEnzyme InhibitorsHistone Deacetylase 3Histone DeacetylasesImidazolesLosartanp38 Mitogen-Activated Protein KinasesPPAR gammaPyridinesReceptor, Angiotensin, Type 1RNA, MessengerRNA, Small InterferingSB 203580Transforming Growth Factor beta1

Identifiers

PMID22095985
PMCPMC3262055
OpenAlexW2156936473

What OpenQuestion holds

Textmetadata
LicenceTDM
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.