Evidence map›Paper›PMID 25870279›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

Increased size and cellularity of advanced atherosclerotic lesions in mice with endothelial overexpression of the human TRPC3 channel.

Kathryn B Smedlund, Lutz Birnbaumer, Guillermo Vazquez

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. 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
2.4field-weighted citation impact, top 11% 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, 33 citations in OpenAlex.

  1. Review
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  8. Role of mechanosensitive channels/receptors in atherosclerosis.American journal of physiology. Cell physiology · 2022
    Review
  9. Article
  10. Review
  11. TRPC and TRPV Channels' Role in Vascular Remodeling and Disease.International journal of molecular sciences · 2020
    Review
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  13. Article
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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

3 authors at 2 institutions in 1 country.

Kathryn B SmedlundDepartment of Physiology and Pharmacology, Center for Diabetes and Endocrine Research, University of Toledo College of Medicine, Toledo, OH 43614; and.
Lutz BirnbaumerNeurobiology Laboratory, National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709 birnbau1@niehs.nih.gov Guillermo.Vazquez@utoledo.edu.
Guillermo VazquezDepartment of Physiology and Pharmacology, Center for Diabetes and Endocrine Research, University of Toledo College of Medicine, Toledo, OH 43614; and birnbau1@niehs.nih.gov Guillermo.Vazquez@utoledo.edu.
University of Toledo · USNational Institutes of Health · US

Funding

TRPC3 Channels in Molecular and Cellular Events of AtherogenesisR01HL111877 · NHLBI · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI VAZQUEZ, GUILLERMO · 2012 to 2015
$1.5M
Intramural NIH HHSNHLBI NIH HHS R01 HL111877NHLBI NIH HHS R01HL111877-03NIEHS NIH HHS Z01-ES-101864
6 · The paper itself

Abstract

In previous in vitro studies, we showed that Transient Receptor Potential Canonical 3 (TRPC3), a calcium-permeable, nonselective cation channel endowed with high constitutive function, is an obligatory component of the inflammatory signaling that controls expression of the vascular cell adhesion molecule-1 (VCAM-1) and monocyte adhesion to coronary artery endothelial cells. Also, TRPC3 expression in these cells was found to be up-regulated by proatherogenic factors, which enhanced inflammation and VCAM-1 expression. However, it remained to be determined whether these in vitro findings were of relevance to atherosclerotic lesion development in vivo. To answer this important question in the present work, we generated mice with endothelial-specific overexpression of human TRPC3 in an Apoe knockout background (TgEST3ApoeKO) and examined lesions in the aortic sinus following 10 and 16 wk on a high-fat diet. No significant differences were found in size or complexity of early stage lesions (10 wk). However, advanced plaques (16 wk) from TgEST3ApoeKO mice exhibited a significant increase in size and macrophage content compared with nontransgenic littermate controls. Remarkably, this change was correlated with increased VCAM-1 and phospho-IkBα immunoreactivity along the endothelial lining of lesions from transgenic animals compared with controls. These findings validate the in vivo relevance of previous in vitro findings and represent, to our knowledge, the first in vivo evidence for a proatherogenic role of endothelial TRPC3.

Indexed as

AnimalsApolipoproteins EAtherosclerosisEndothelium, VascularGene ExpressionHumansI-kappa B KinaseMacrophagesMiceMice, TransgenicPlaque, AtheroscleroticTRPC Cation ChannelsVascular Cell Adhesion Molecule-1Apolipoproteins EI-kappa B KinaseTRPC3 cation channelTRPC Cation ChannelsVascular Cell Adhesion Molecule-1atherosclerosisendothelial inflammationTRPC3 channels

Identifiers

PMID25870279
PMCPMC4418920
OpenAlexW1984098907

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.