Evidence map›Paper›PMID 20519447›Full record

ArticleAmerican journal of physiology. Cell physiology2010

Mitochondrial depolarization underlies delay in permeability transition by preconditioning with isoflurane: roles of ROS and Ca2+.

Filip Sedlic, Ana Sepac, Danijel Pravdic, Amadou K S Camara, Martin Bienengraeber, Anna K Brzezinska, Tetsuro Wakatsuki, Zeljko J Bosnjak

Open access · greenAbstract readComparative Study
In one paragraph

Article in American journal of physiology. Cell physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

42 citing papers in PubMed, 81 citations in OpenAlex.

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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

8 authors at 1 institution in 1 country.

Filip SedlicDepartment of Anesthesiology and Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin53226, USA. fsedlic@mcw.edu
Ana Sepac
Danijel Pravdic
Amadou K S Camara
Martin Bienengraeber
Anna K Brzezinska
Tetsuro Wakatsuki
Zeljko J Bosnjak
Medical College of Wisconsin · US

Funding

Stem Cell CoreP01GM066730 · NIGMS · MEDICAL COLLEGE OF WISCONSIN · PI DASH, RANJAN K · 2003 to 2019
$23.6M
INTERACTION BETWEEN ANESTHETICS AND CALCIUM ANTAGONISTSR01HL034708 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI BOSNJAK, ZELJKO J. · 1986 to 2013
$3.9M
NHLBI NIH HHS R01HL034708NIGMS NIH HHS P01 GM066730NIGMS NIH HHS P01GM066730
6 · The paper itself

Abstract

During reperfusion, the interplay between excess reactive oxygen species (ROS) production, mitochondrial Ca(2+) overload, and mitochondrial permeability transition pore (mPTP) opening, as the crucial mechanism of cardiomyocyte injury, remains intriguing. Here, we investigated whether an induction of a partial decrease in mitochondrial membrane potential (DeltaPsi(m)) is an underlying mechanism of protection by anesthetic-induced preconditioning (APC) with isoflurane, specifically addressing the interplay between ROS, Ca(2+), and mPTP opening. The magnitude of APC-induced decrease in DeltaPsi(m) was mimicked with the protonophore 2,4-dinitrophenol (DNP), and the addition of pyruvate was used to reverse APC- and DNP-induced decrease in DeltaPsi(m). In cardiomyocytes, DeltaPsi(m), ROS, mPTP opening, and cytosolic and mitochondrial Ca(2+) were measured using confocal microscope, and cardiomyocyte survival was assessed by Trypan blue exclusion. In isolated cardiac mitochondria, antimycin A-induced ROS production and Ca(2+) uptake were determined spectrofluorometrically. In cells exposed to oxidative stress, APC and DNP increased cell survival, delayed mPTP opening, and attenuated ROS production, which was reversed by mitochondrial repolarization with pyruvate. In isolated mitochondria, depolarization by APC and DNP attenuated ROS production, but not Ca(2+) uptake. However, in stressed cardiomyocytes, a similar decrease in DeltaPsi(m) attenuated both cytosolic and mitochondrial Ca(2+) accumulation. In conclusion, a partial decrease in DeltaPsi(m) underlies cardioprotective effects of APC by attenuating excess ROS production, resulting in a delay in mPTP opening and an increase in cell survival. Such decrease in DeltaPsi(m) primarily attenuates mitochondrial ROS production, with consequential decrease in mitochondrial Ca(2+) uptake.

Indexed as

AnimalsCalciumCytoprotectionIsofluraneMaleMembrane Potential, MitochondrialMitochondria, HeartMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreRatsRats, WistarReactive Oxygen SpeciesTime FactorsCalciumIsofluraneMitochondrial Membrane Transport ProteinsMitochondrial Permeability Transition PoreReactive Oxygen Species

Identifiers

PMID20519447
PMCPMC2928640
OpenAlexW2118491346

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.