Evidence map›Paper›PMID 20648037›Full record

ArticleJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism2011

Neuroprotective signaling pathways are modulated by adenosine in the anoxia tolerant turtle.

Gauri H Nayak, Howard M Prentice, Sarah L Milton

Open access · hybridAbstract read
In one paragraph

Article in Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism, 2011. 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
2.2field-weighted citation impact, top 15% 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, 35 citations in OpenAlex.

  1. Article
  2. Carbon dioxide and MAPK signalling: towards therapy for inflammation.Cell communication and signaling : CCS · 2023
    Review
  3. Review
  4. Article
  5. Induction of foxo3a protects turtle neurons against oxidative stress.Comparative biochemistry and physiology. Part A, Molecular & integrative physiology · 2020
    Article
  6. Review
  7. Comparative Response of Brain to Chronic Hypoxia and Hyperoxia.International journal of molecular sciences · 2017
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Mitochondria from anoxia-tolerant animals reveal common strategies to survive without oxygen.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2014
    Review
  15. Review
  16. Review
  17. Article
  18. 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

3 authors at 2 institutions in 1 country.

Gauri H NayakDepartment of Biology, Boston University, Boston, Massachusetts 02215, USA. gnayak@bu.edu
Howard M Prentice
Sarah L Milton
Florida Atlantic University · USBoston University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cumulative evidence shows a protective role for adenosine A1 receptors (A1R) in hypoxia/ischemia; A1R stimulation reduces neuronal damage, whereas blockade exacerbates damage. The signal transduction pathways may involve the mitogen-activated protein kinase (MAPK) pathways and serine/threonine kinase (AKT), with cell survival depending on the timing and degree of upregulation of these cascades as well as the balance between pro-survival and pro-death pathways. Here, we show in vitro that extracellular signal-regulated kinase (ERK1/2) and phosphatidylinositol 3-kinase (PI3-K/AKT) activation is dependent on A1R stimulation, with further downstream effects that promote neuronal survival. Phosphorylated ERK1/2 (p-ERK) and AKT (p-AKT) as well as Bcl-2 are upregulated in anoxic neuronally enriched primary cultures from turtle brain. This native upregulation is further increased by the selective A1R agonist 2-chloro-N-cyclopentyladenosine (CCPA), whereas the selective antagonist 8-cyclopentyl-1,3-dihydropylxanthine (DPCPX) decreases p-ERK and p-AKT expression. Conversely, A1R antagonism resulted in increases in phosphorylated JNK (p-JNK), p38 (p-p38), and Bax. As pathological and adaptive changes occur simultaneously during anoxia/ischemia in mammalian neurons, the turtle provides an alternative model to analyze protective mechanisms in the absence of evident pathologies.

Indexed as

Neuroprotective AgentsAdenosineAdenosine A1 Receptor AgonistsAdenosine A1 Receptor AntagonistsAnimalsApoptosisbcl-2-Associated X ProteinBlotting, WesternCells, CulturedCell SurvivalHypoxiaImmunohistochemistryJanus KinasesMitogen-Activated Protein KinasesNeuronsp38 Mitogen-Activated Protein KinasesAdenosineAdenosine A1 Receptor AgonistsAdenosine A1 Receptor Antagonistsbcl-2-Associated X ProteinJanus KinasesMitogen-Activated Protein KinasesNeuroprotective Agentsp38 Mitogen-Activated Protein KinasesPhosphoproteinsProto-Oncogene Proteins c-aktProto-Oncogene Proteins c-bcl-2

Identifiers

PMID20648037
PMCPMC3049502
OpenAlexW2036231596

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.