Evidence map›Paper›PMID 23050650›Full record

ArticleJournal of neurochemistry2012

Mitochondrial biogenesis contributes to ischemic neuroprotection afforded by LPS pre-conditioning.

R Anne Stetler, Rehana K Leak, Wei Yin, Lili Zhang, Suping Wang, Yanqin Gao, Jun Chen

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

24 citing papers in PubMed, 59 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

7 authors at 3 institutions in 2 countries.

R Anne StetlerState Key Laboratory of Medical Neurobiology and Institute of Brain Sciences, Shanghai, China.
Rehana K Leak
Wei Yin
Lili Zhang
Suping Wang
Yanqin Gao
Jun Chen
Institute of Neurobiology · BGUniversity of Pittsburgh · USDuquesne University · US

Funding

Stress Proteins and Neuroprotection Against Parkinsonian Cell DeathP01NS059806 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI HASTINGS, TERESA G · 2009 to 2013
$6.3M
INDUCIBLE DNA REPAIR IN CEREBRAL ISCHEMIAR01NS036736 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI BENNETT, MICHAEL V L, GRAHAM, STEVEN H · 1997 to 2021
$5.4M
Neuroprotection in Models of Cerebral IschemiaR01NS045048 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, JUN · 2003 to 2015
$3.1M
Neuroprotection Against Parkinsonian Cell DeathR01NS062157 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, JUN · 2010 to 2014
$1.5M
Neuroprotective effect of HSP27 in Cerebral IschemiaR01NS056118 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, JUN · 2006 to 2010
$1.5M
Programmed Cell Death Induced by Cerebral IschemiaR01NS043802 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI CHEN, JUN · 2002 to 2006
$1.4M
NINDS NIH HHS NS36736NINDS NIH HHS NS43802NINDS NIH HHS NS45048NINDS NIH HHS NS56118NINDS NIH HHS P01 NS059806NINDS NIH HHS R01 NS036736NINDS NIH HHS R01 NS043802NINDS NIH HHS R01 NS045048NINDS NIH HHS R01 NS056118NINDS NIH HHS R01 NS062157
6 · The paper itself

Abstract

Although alterations in mitochondrial dynamics are associated with cellular responses to injury, the functional role of these dynamic changes in ischemic neurons is underexplored. One of these dynamic responses to injury includes mitochondrial biogenesis. Various sublethal pre-conditioning stimuli that induce an ischemic-tolerant state [e.g., lipopolysaccharide (LPS)] may also induce mitochondrial biogenesis. Using neuron-enriched cultures, we found that sublethal LPS pre-conditioning induced both ischemic tolerance and markers of mitochondrial biogenesis with overlapping dose-response temporal kinetics. Sublethal LPS transiently increased the expression of critical components of the mitochondrial transcriptional machinery, including nuclear respiratory factor 1 (NRF1) and mitochondrial transcription factor A (TFAM), as well as mtDNA copy number, mitochondrial protein levels, and markers of functional mitochondria, such as increased cellular ATP content, citrate synthase activity, and maximal respiration capacity. Importantly, knockdown of TFAM abrogated both the induction of mitochondrial biogenesis and the neuroprotective pre-conditioning effects of LPS. Several signaling pathways coordinated these events. AMPK inhibition suppressed NRF1 and TFAM expression by LPS, whereas PI3K/Akt signaling was necessary for the nuclear translocation of NRF1 and subsequent induction of TFAM. This is the first demonstration that LPS pre-conditioning initiates multiple signaling pathways leading to mitochondrial biogenesis in neurons and that these dynamic changes contribute to ischemic tolerance.

Indexed as

Adenosine TriphosphateAMP-Activated Protein Kinase KinasesAnalysis of VarianceAnimalsCell CountCells, CulturedCerebral CortexCitrate (si)-SynthaseDNA-Binding ProteinsDNA, MitochondrialDrug Administration ScheduleEmbryo, MammalianEnzyme InhibitorsGene Expression RegulationGenetic VectorsGlucoseAdenosine TriphosphateAMP-Activated Protein Kinase KinasesCitrate (si)-SynthaseDNA-Binding ProteinsDNA, MitochondrialdorsomorphinEnzyme InhibitorsGlucoseLipopolysaccharidesMitochondrial Proteinsmitochondrial transcription factor ANeuroprotective AgentsNuclear Respiratory Factor 1Oncogene Protein v-aktPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPpargc1a protein, ratProtein KinasesPyrazolesPyrimidinesRNA-Binding ProteinsRNA, MessengerRNA, Small InterferingTranscription Factors

Identifiers

PMID23050650
PMCPMC3623612
OpenAlexW2019488837

What OpenQuestion holds

Textmetadata
LicenceTDM
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.