Evidence map›Paper›PMID 19709640›Full record

ArticleCellular signalling2009

Lysophosphatidic acid-induced arterial wall remodeling: requirement of PPARgamma but not LPA1 or LPA2 GPCR.

Yunhui Cheng, Natalia Makarova, Ryoko Tsukahara, Huazhang Guo, E Shuyu, Patricia Farrar, Louisa Balazs, Chunxiang Zhang, Gabor Tigyi

Open access · greenAbstract read
In one paragraph

Article in Cellular signalling, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

23 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Pathogenesis of Systemic Sclerosis.Frontiers in immunology · 2015
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Lysophosphatidic acid in atherosclerotic diseases.British journal of pharmacology · 2012
    Review
  19. Review
  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

9 authors at 1 institution in 1 country.

Yunhui ChengDepartment of Physiology, University of Tennessee Health Science Center, 894 Union Ave., Suite 426, Memphis, TN 38163, USA.
Natalia Makarova
Ryoko Tsukahara
Huazhang Guo
E Shuyu
Patricia Farrar
Louisa Balazs
Chunxiang Zhang
Gabor Tigyi
University of Tennessee Health Science Center · US

Funding

Ligand Recognition by Phospholipid Growth Factor ReceptorsR01CA092160 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI TIGYI, GABOR J · 2001 to 2022
$5.9M
Role of miR-145 in Vascular Smooth Muscle Cell BiologyRole ofR01HL095707 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ZHANG, CHUNXIANG · 2010 to 2013
$1.5M
MPO and NO signaling in neointima formationR01HL080133 · NHLBI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI ZHANG, CHUNXIANG · 2006 to 2010
$1.5M
Analysis of LPA Signaling through the GPCR-PPARgamma AxisR01HL079004 · NHLBI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI TIGYI, GABOR J · 2005 to 2008
$1.4M
NCI NIH HHS R01 CA092160NHLBI NIH HHS HL79004NHLBI NIH HHS R01 HL079004NHLBI NIH HHS R01 HL080133NHLBI NIH HHS R01 HL095707
6 · The paper itself

Abstract

Lysophosphatidic acid (LPA) and its ether analog alkyl-glycerophosphate (AGP) elicit arterial wall remodeling when applied intralumenally into the uninjured carotid artery. LPA is the ligand of eight GPCRs and the peroxisome proliferator-activated receptor gamma (PPARgamma). We pursued a gene knockout strategy to identify the LPA receptor subtypes necessary for the neointimal response in a non-injury model of carotid remodeling and also compared the effects of AGP and the PPARgamma agonist rosiglitazone (ROSI) on balloon injury-elicited neointima development. In the balloon injury model AGP significantly increased neointima; however, rosiglitazone application attenuated it. AGP and ROSI were also applied intralumenally for 1h without injury into the carotid arteries of LPA(1), LPA(2), LPA(1&2) double knockout, and Mx1Cre-inducible conditional PPARgamma knockout mice targeted to vascular smooth muscle cells, macrophages, and endothelial cells. The neointima was quantified and also stained for CD31, CD68, CD11b, and alpha-smooth muscle actin markers. In LPA(1), LPA(2), LPA(1&2) GPCR knockout, Mx1Cre transgenic, PPARgamma(fl/-), and uninduced Mx1CrexPPARgamma(fl/-) mice AGP- and ROSI-elicited neointima was indistinguishable in its progression and cytological features from that of WT C57BL/6 mice. In PPARgamma(-/-) knockout mice, generated by activation of Mx1Cre-mediated recombination, AGP and ROSI failed to elicit neointima and vascular wall remodeling. Our findings point to a difference in the effects of AGP and ROSI between the balloon injury- and the non-injury chemically-induced neointima. The present data provide genetic evidence for the requirement of PPARgamma in AGP- and ROSI-elicited neointimal thickening in the non-injury model and reveal that the overwhelming majority of the cells in the neointimal layer express alpha-smooth muscle actin.

Indexed as

AnimalsCarotid Artery, CommonCarotid Artery InjuriesGene Knockdown TechniquesGlycerophosphatesHypoglycemic AgentsLysophospholipidsMaleMiceMice, Inbred C57BLMice, KnockoutPPAR gammaRatsRats, Sprague-DawleyReceptors, G-Protein-CoupledRosiglitazoneGlycerophosphatesHypoglycemic Agentslysophosphatidic acidLysophospholipidsPPAR gammaReceptors, G-Protein-CoupledRosiglitazoneThiazolidinediones

Identifiers

PMID19709640
PMCPMC2760670
OpenAlexW2014609417

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.