Evidence map›Paper›PMID 25265380›Full record

ArticlePloS one2014

Glucocorticoid modulates angiotensin II receptor expression patterns and protects the heart from ischemia and reperfusion injury.

Qin Xue, Andrew J Patterson, Daliao Xiao, Lubo Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. 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
1.7field-weighted citation impact, top 16% 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, 38 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Estrogen normalizes maternal HFD-induced vascular dysfunction in offspring by regulating ATR.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Article
  5. Article
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  8. Review
  9. Maternal high-fat diet increases vascular contractility in adult offspring in a sex-dependent manner.Hypertension research : official journal of the Japanese Society of Hypertension · 2021
    Article
  10. Review
  11. Hurdles to Cardioprotection in the Critically Ill.International journal of molecular sciences · 2019
    Review
  12. Article
  13. Review
  14. Article
  15. 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

4 authors at 1 institution in 1 country.

Qin XueCenter for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California, United States of America.
Andrew J PattersonCenter for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California, United States of America.
Daliao XiaoCenter for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California, United States of America.
Lubo ZhangCenter for Perinatal Biology, Division of Pharmacology, Department of Basic Sciences, Loma Linda University School of Medicine, Loma Linda, California, United States of America.
Loma Linda University · US

Funding

Maternal Hypoxia and Programming of Fetal HeartR01HL083966 · NHLBI · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 2007 to 2011
$1.8M
Developmental Programming of Ischemic-Sensitive Phenotype in the HeartR01HL118861 · NHLBI · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 2014 to 2017
$1.8M
Prenatal Cocaine Exposure and Cardiac ProgrammingR01HL082779 · NHLBI · LOMA LINDA UNIVERSITY · PI ZHANG, LUBO · 2006 to 2009
$1.6M
NHLBI NIH HHS HL082779NHLBI NIH HHS HL083966NHLBI NIH HHS HL118861NHLBI NIH HHS R01 HL082779NHLBI NIH HHS R01 HL083966NHLBI NIH HHS R01 HL118861
6 · The paper itself

Abstract

Glucocorticoid regulates angiotensin II receptor (ATR) expression via activating glucocorticoid receptors and binding to glucocorticoid response elements. The regulation of ATR by glucocorticoids in the context of myocardial injury from ischemia/reperfusion (I/R) is yet to be elucidated. The present study determined the role of ATR in glucocorticoid-induced cardiac protection. Adult male rats were administered once a day i.p. 1 mg/kg/day dexamethasone or dexamethasone plus 10 mg/kg/day RU486 for 5 days. Hearts were then isolated and subjected to I/R injury in a Langendorff preparation. Dexamethasone treatment significantly decreased I/R injury and improved post-ischemic recovery of cardiac function. Dexamethasone increased glucocorticoid receptor binding to glucocorticoid response elements at AT1aR and AT2R promoters, resulting in a significant increase in expression of AT1R protein but a decrease in AT2R expression in the heart. In addition, dexamethasone treatment significantly increased PKCε expression and p-PKCε protein abundance. These dexamethasone-mediated effects were blocked by RU486. More importantly, blockade of AT1R and AT2R with losartan and PD123319 abrogated dexamethasone-induced protection of the heart from I/R injury. The results indicate that glucocorticoid promotes a cardioprotective phenotype associated with the upregulation of AT1R and PKCε and downregulation of AT2R in the heart.

Indexed as

AnimalsChromatin ImmunoprecipitationDexamethasoneDown-RegulationElectrophoretic Mobility Shift AssayGene Expression RegulationMaleMyocardial Reperfusion InjuryPromoter Regions, GeneticProtein Kinase C-epsilonRatsRats, Sprague-DawleyReal-Time Polymerase Chain ReactionReceptors, AngiotensinReperfusion InjuryUp-RegulationDexamethasoneProtein Kinase C-epsilonReceptors, Angiotensin

Identifiers

PMID25265380
PMCPMC4180065
OpenAlexW2076270873

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.