Evidence map›Paper›PMID 25069723›Full record

ArticleMolecular pharmacology2014

Regulation of mitochondrial poly(ADP-Ribose) polymerase activation by the β-adrenoceptor/cAMP/protein kinase A axis during oxidative stress.

Attila Brunyanszki, Gabor Olah, Ciro Coletta, Bartosz Szczesny, Csaba Szabo

Open access · greenAbstract read
In one paragraph

Article in Molecular pharmacology, 2014. 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
1.2field-weighted citation impact, top 24% 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, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. NADAntioxidants (Basel, Switzerland) · 2023
    Review
  7. Review
  8. Mitochondrial PARP1 regulates NADExperimental & molecular medicine · 2022
    Article
  9. Article
  10. Article
  11. Review
  12. A ribose-functionalized NADNature communications · 2019
    Article
  13. Review
  14. Review
  15. Article
  16. An Effective Epigenetic-PARP Inhibitor Combination Therapy for Breast and Ovarian Cancers Independent of BRCA Mutations.Clinical cancer research : an official journal of the American Association for Cancer Research · 2018
    Article
  17. Article
  18. Review
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Attila BrunyanszkiDepartment of Anesthesiology, University of Texas Medical Branch, Galveston, Texas.
Gabor OlahDepartment of Anesthesiology, University of Texas Medical Branch, Galveston, Texas.
Ciro ColettaDepartment of Anesthesiology, University of Texas Medical Branch, Galveston, Texas.
Bartosz SzczesnyDepartment of Anesthesiology, University of Texas Medical Branch, Galveston, Texas.
Csaba SzaboDepartment of Anesthesiology, University of Texas Medical Branch, Galveston, Texas szabocsaba@aol.com.
The University of Texas Medical Branch at Galveston · US

Funding

Project 9: The role of androgen/corticosteroid in fat, muscle and glucose metabolism of burn victimsP50GM060338 · NIGMS · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI HERNDON, DAVID N. · 2000 to 2017
$24.2M
NIGMS NIH HHS GM060338NIGMS NIH HHS P50 GM060338
6 · The paper itself

Abstract

We investigated the regulation of mitochondrial poly(ADP-ribose) polymerase 1 (PARP1) by the cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA) system during oxidative stress in U937 monocytes. Oxidative stress induced an early (10 minutes) mitochondrial DNA damage, and concomitant activation of PARP1 in the mitochondria. These early events were followed by a progressive mitochondrial oxidant production and nuclear PARP1 activation (by 6 hours). These processes led to a functional impairment of mitochondria, culminating in cell death of mixed (necrotic/apoptotic) type. β-Adrenoceptor blockade with propranolol or inhibition of its downstream cAMP/PKA signaling attenuated, while β-adrenoceptor agonists and cAMP/PKA activators enhanced, the oxidant-mediated PARP1 activation. In the presence of cAMP, recombinant PKA directly phosphorylated recombinant PARP1 on serines 465 (in the automodification domain) and 782 and 785 (both in the catalytic domain). Inhibition of the β-adrenergic receptor/cAMP/PKA axis protected against the oxidant-mediated cell injury. Propranolol also suppressed PARP1 activation in peripheral blood leukocytes during bacterial lipopolysaccharide (LPS)-induced systemic inflammation in mice. We conclude that the activation of mitochondrial PARP1 is an early, active participant in oxidant-induced cell death, which is under the control of β-adrenoceptor/cAMP/PKA axis through the regulation of PARP1 activity by PARP1 phosphorylation.

Indexed as

Oxidative StressAdrenergic beta-AntagonistsAnimalsApoptosisCell LineCell Line, TumorCyclic AMPCyclic AMP-Dependent Protein KinasesDNA DamageDNA, MitochondrialHumansInflammationLeukocytesLipopolysaccharidesMiceMitochondrial ProteinsAdrenergic beta-AntagonistsCyclic AMPCyclic AMP-Dependent Protein KinasesDNA, MitochondrialLipopolysaccharidesMitochondrial ProteinsPoly(ADP-ribose) PolymerasesPropranololReceptors, Adrenergic, beta

Identifiers

PMID25069723
PMCPMC4164979
OpenAlexW2132308872

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.