Evidence map›Paper›PMID 29552233›Full record

ArticleCellular and molecular bioengineering2017

Cyclic Strain and Hypertension Increase Osteopontin Expression in the Aorta.

Christa Caesar, Alicia N Lyle, Giji Joseph, Daiana Weiss, Fadi M F Alameddine, Bernard Lassègue, Kathy K Griendling, W Robert Taylor

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular bioengineering, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
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  8. Article
  9. Review
  10. Article
  11. Osteopontin in Vascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Article
  12. Article
  13. Review
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

8 authors at 3 institutions in 1 country.

Christa CaesarDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Alicia N LyleDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Giji JosephDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Daiana WeissDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Fadi M F AlameddineDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Bernard LassègueDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Kathy K GriendlingDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
W Robert TaylorDivision of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Emory University · USThe Wallace H. Coulter Department of Biomedical Engineering · USVeterans Health Administration · US

Funding

T cell triggering events and hypertensionP01HL095070 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG · 2009 to 2019
$20.5M
NHLBI NIH HHS P01 HL095070
6 · The paper itself

Abstract

Hypertension has a direct impact on vascular hypertrophy and is a known risk factor for the development of atherosclerosis. Osteopontin (OPN) has emerged as an important protein mediator of inflammation and remodeling of large arteries. However, its role and mechanism of regulation in the setting of hypertension is still unknown. Our objectives for this study were therefore to investigate the role of OPN in hypertension-induced vascular remodeling and inflammation. OPN Knockout (KO) and wild type (WT) mice were made hypertensive with angiotensin II (Ang II) infusion for seven days. We observed that OPN KO aortas were protected against Ang II-induced medial hypertrophy and inflammation, despite comparable increases in systolic blood pressure (SBP) in both groups. OPN expression was increased in WT aortas from hypertensive mice (induced by either Ang II or norepinephrine). OPN expression was increased in aortic smooth muscle cells (SMCs) subjected to cyclic mechanical strain suggesting that mechanical deformation of the aortic wall is responsible in part for the increased OPN expression induced by hypertension. Finally, we utilized hypertensive transgenic smooth muscle cell-specific catalase overexpressing (Tg

Indexed as

Angiotensin IICyclic strainInflammationNorepinephrineSmooth muscle cellsVascular hypertrophy

Identifiers

PMID29552233
PMCPMC5851655
OpenAlexW2566290192

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.