Evidence map›Paper›PMID 26084308›Full record

ArticleAmerican journal of physiology. Cell physiology2015

Stimulation of the cardiac myocyte Na+-K+ pump due to reversal of its constitutive oxidative inhibition.

Karin K M Chia, Chia-Chi Liu, Elisha J Hamilton, Alvaro Garcia, Natasha A Fry, William Hannam, Gemma A Figtree, Helge H Rasmussen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Pivotal role of α2 NaThe Journal of physiology · 2016
    Review
  6. Article
  7. Review
  8. 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

8 authors at 1 institution in 1 country.

Karin K M ChiaNorth Shore Heart Research Group, Kolling Medical Research Institute, University of Sydney, Sydney, Australia; Royal Brisbane and Women's Hospital, The University of Queensland, Queensland, Australia; and.
Chia-Chi LiuNorth Shore Heart Research Group, Kolling Medical Research Institute, University of Sydney, Sydney, Australia;
Elisha J HamiltonNorth Shore Heart Research Group, Kolling Medical Research Institute, University of Sydney, Sydney, Australia;
Alvaro GarciaNorth Shore Heart Research Group, Kolling Medical Research Institute, University of Sydney, Sydney, Australia;
Natasha A FryNorth Shore Heart Research Group, Kolling Medical Research Institute, University of Sydney, Sydney, Australia;
William HannamNorth Shore Heart Research Group, Kolling Medical Research Institute, University of Sydney, Sydney, Australia;
Gemma A FigtreeNorth Shore Heart Research Group, Kolling Medical Research Institute, University of Sydney, Sydney, Australia; Department of Cardiology, Royal North Shore Hospital, St. Leonards, Australia.
Helge H RasmussenNorth Shore Heart Research Group, Kolling Medical Research Institute, University of Sydney, Sydney, Australia; Department of Cardiology, Royal North Shore Hospital, St. Leonards, Australia helge.rasmussen@sydney.edu.au.
University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Protein kinase C can activate NADPH oxidase and induce glutathionylation of the β1-Na(+)-K(+) pump subunit, inhibiting activity of the catalytic α-subunit. To examine if signaling of nitric oxide-induced soluble guanylyl cyclase (sGC)/cGMP/protein kinase G can cause Na(+)-K(+) pump stimulation by counteracting PKC/NADPH oxidase-dependent inhibition, cardiac myocytes were exposed to ANG II to activate NADPH oxidase and inhibit Na(+)-K(+) pump current (Ip). Coexposure to 3-(5'-hydroxymethyl-2'-furyl)-1-benzylindazole (YC-1) to stimulate sGC prevented the decrease of Ip. Prevention of the decrease was abolished by inhibition of protein phosphatases (PP) 2A but not by inhibition of PP1, and it was reproduced by an activator of PP2A. Consistent with a reciprocal relationship between β1-Na(+)-K(+) pump subunit glutathionylation and pump activity, YC-1 decreased ANG II-induced β1-subunit glutathionylation. The decrease induced by YC-1 was abolished by a PP2A inhibitor. YC-1 decreased phosphorylation of the cytosolic p47(phox) NADPH oxidase subunit and its coimmunoprecipitation with the membranous p22(phox) subunit, and it decreased O2 (·-)-sensitive dihydroethidium fluorescence of myocytes. Addition of recombinant PP2A to myocyte lysate decreased phosphorylation of p47(phox) indicating the subunit could be a substrate for PP2A. The effects of YC-1 to decrease coimmunoprecipitation of p22(phox) and p47(phox) NADPH oxidase subunits and decrease β1-Na(+)-K(+) pump subunit glutathionylation were reproduced by activation of nitric oxide-dependent receptor signaling. We conclude that sGC activation in cardiac myocytes causes a PP2A-dependent decrease in NADPH oxidase activity and a decrease in β1 pump subunit glutathionylation. This could account for pump stimulation with neurohormonal oxidative stress expected in vivo.

Indexed as

AnimalsCells, CulturedEnzyme InhibitorsMyocytes, CardiacOxidation-ReductionOxidative StressProtein Phosphatase 2RabbitsSodium-Potassium-Exchanging ATPaseEnzyme InhibitorsProtein Phosphatase 2Sodium-Potassium-Exchanging ATPaseglutathionylationnitric oxideoxidative stresssodium-potassium (Na+-K+)-ATPasesoluble guanylyl cyclase

Identifiers

PMID26084308
PMCPMC4537930
OpenAlexW2141393274

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.