Evidence map›Paper›PMID 24375799›Full record

ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014

Dehydroepiandrosterone promotes pulmonary artery relaxation by NADPH oxidation-elicited subunit dimerization of protein kinase G 1α.

Dhara Patel, Sharath Kandhi, Melissa Kelly, Boon Hwa Neo, Michael S Wolin

Abstract read
In one paragraph

Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  8. Dehydroepiandrosterone inhibits IAmerican journal of physiology. Heart and circulatory physiology · 2018
    Article
  9. Emerging therapeutics in pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2018
    Review
  10. Article
  11. Review
  12. Update on novel targets and potential treatment avenues in pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2016
    Review
  13. Article
  14. 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

5 authors at 1 institution in 1 country.

Dhara PatelDept. of Physiology, New York Medical College, Valhalla, NY 10595. mike_wolin@nymc.edu).
Sharath Kandhi
Melissa Kelly
Boon Hwa Neo
Michael S Wolin
New York Medical College · US

Funding

VASCULAR REGULATION BY FLOW VELOCITY/ENDOTHELIUMP01HL043023 · NHLBI · NEW YORK MEDICAL COLLEGE · PI KALEY, GABOR · 1991 to 2011
$19.5M
REACTIVE OXYGEN SPECIES AND VASCULAR O2 SENSINGR01HL066331 · NHLBI · NEW YORK MEDICAL COLLEGE · PI WOLIN, MICHAEL S · 2000 to 2010
$2.7M
ecSOD derived peroxide in pulmonary adaptation to hypoxiaR01HL115124 · NHLBI · NEW YORK MEDICAL COLLEGE · PI WOLIN, MICHAEL S · 2013 to 2016
$1.6M
PULMONARY VASODILATION AND GUANYLATE CYCLASE REGULATIONR01HL031069 · NHLBI · NEW YORK MEDICAL COLLEGE · PI WOLIN, MICHAEL S · 1987 to 2010
$1.4M
NHLBI NIH HHS P01 HL043023NHLBI NIH HHS P01HL043023NHLBI NIH HHS R01 HL031069NHLBI NIH HHS R01HL031069NHLBI NIH HHS R01 HL066331NHLBI NIH HHS R01HL066331NHLBI NIH HHS R01 HL115124NHLBI NIH HHS R01HL115124
6 · The paper itself

Abstract

The activity of glucose-6-phosphate dehydrogenase (G6PD) controls a vascular smooth muscle relaxing mechanism promoted by the oxidation of cytosolic NADPH, which has been associated with activation of the 1α form of protein kinase G (PKG-1α) by a thiol oxidation-elicited subunit dimerization. This PKG-1α-activation mechanism appears to contribute to responses of isolated endothelium-removed bovine pulmonary arteries (BPA) elicited by peroxide, cytosolic NADPH oxidation resulting from G6PD inhibition, and hypoxia. Dehydroepiandrosterone (DHEA) is a steroid hormone with pulmonary vasodilator activity, which has beneficial effects in treating pulmonary hypertension. Because multiple mechanisms have been suggested for the vascular effects of DHEA and one of the known actions of DHEA is inhibiting G6PD, we investigated whether it promoted relaxation associated with NADPH oxidation, PKG-1α dimerization, and PKG activation detected by increased vasodilator-stimulated phosphoprotein (VASP) phosphorylation. Relaxation of BPA to DHEA under aerobic or hypoxic conditions was associated with NADPH oxidation, PKG-1α dimerization, and increased VASP phosphorylation. The vasodilator activity of DHEA was markedly attenuated in pulmonary arteries and aorta from a PKG knockin mouse containing a serine in place of a cysteine involved in PKG dimerization. DHEA promoted increased PKG dimerization in lungs from wild-type mice, which was not detected in the PKG knockin mouse model. Thus PKG-1α dimerization is a major contributing factor to the vasodilator actions of DHEA and perhaps its beneficial effects in treating pulmonary hypertension.

Indexed as

VasodilationAcetylcholineAnimalsCattleCell Adhesion MoleculesCell HypoxiaCyclic GMP-Dependent Protein Kinase Type IDehydroepiandrosteroneGlucosephosphate DehydrogenaseHydrogen PeroxideIn Vitro TechniquesLungMiceMice, TransgenicMicrofilament ProteinsNADPAcetylcholineCell Adhesion MoleculesCyclic GMP-Dependent Protein Kinase Type IDehydroepiandrosteroneGlucosephosphate DehydrogenaseHydrogen PeroxideMicrofilament ProteinsNADPNADPH OxidasesPhosphoproteinsProtein SubunitsSperminespermine nitric oxide complexVasodilator AgentsVasodilator-Stimulated PhosphoproteincGMPglucose-6-phosphate dehydrogenasepulmonary hypertension

Identifiers

PMID24375799
PMCPMC3920223
OpenAlexW1969365096

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.