Evidence map›Paper›PMID 23653362›Full record

ArticleThe Journal of biological chemistry2013

Up-regulation of ciliary neurotrophic factor in astrocytes by aspirin: implications for remyelination in multiple sclerosis.

Khushbu K Modi, Michael Sendtner, Kalipada Pahan

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

39 citing papers in PubMed, 53 citations in OpenAlex.

  1. Trial
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Astrocytic Calcium and cAMP in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022
    Review
  10. Article
  11. Role of glia in optic nerve.Progress in retinal and eye research · 2021
    Review
  12. Review
  13. Article
  14. Review
  15. Low-Dose Aspirin Upregulates Tyrosine Hydroxylase and Increases Dopamine Production in Dopaminergic Neurons: Implications for Parkinson's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
    Article
  16. Article
  17. The Astrocytic cAMP Pathway in Health and Disease.International journal of molecular sciences · 2019
    Review
  18. Article
  19. PPARα Between Aspirin and Plaque Clearance.Journal of Alzheimer's disease : JAD · 2019
    Review
  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

3 authors at 2 institutions in 2 countries.

Khushbu K ModiDepartment of Neurological Sciences, Rush University Medical Center, Chicago, Illinois 60612, USA.
Michael Sendtner
Kalipada Pahan
Rush University Medical Center · USUniversity of Würzburg · DE

Funding

Cinnamon, CNTF and EAER01AT006681 · NCCIH · RUSH UNIVERSITY MEDICAL CENTER · PI PAHAN, KALIPADA · 2011 to 2015
$1.8M
Aspirin, PPAR and EAEI01BX002174 · VA · JESSE BROWN VA MEDICAL CENTER · PI PAHAN, KALIPADA · 2013 to 2016
–
BLRD VA I01 BX002174NCCIH NIH HHS AT6681NCCIH NIH HHS R01 AT006681
6 · The paper itself

Abstract

Ciliary neurotrophic factor (CNTF) is a promyelinating trophic factor, and the mechanisms by which CNTF expression could be increased in the brain are poorly understood. Acetylsalicylic acid (aspirin) is one of the most widely used analgesics. Interestingly, aspirin increased mRNA and protein expression of CNTF in primary mouse and human astrocytes in a dose- and time-dependent manner. Aspirin induced the activation of protein kinase A (PKA) but not protein kinase C (PKC). H-89, an inhibitor of PKA, abrogated aspirin-induced expression of CNTF. The activation of cAMP-response element-binding protein (CREB), but not NF-κB, by aspirin, the abrogation of aspirin-induced expression of CNTF by siRNA knockdown of CREB, the presence of a consensus cAMP-response element in the promoter of CNTF, and the recruitment of CREB and CREB-binding protein to the CNTF promoter by aspirin suggest that aspirin increases the expression of the Cntf gene via the activation of CREB. Furthermore, we demonstrate that aspirin-induced astroglial CNTF was also functionally active and that supernatants of aspirin-treated astrocytes of wild type, but not Cntf null, mice increased myelin-associated proteins in oligodendrocytes and protected oligodendrocytes from TNF-α insult. These results highlight a new and novel myelinogenic property of aspirin, which may be of benefit for multiple sclerosis and other demyelinating disorders.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalApoptosisAspirinAstrocytesCells, CulturedCiliary Neurotrophic FactorCulture Media, ConditionedCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinDose-Response Relationship, DrugGene ExpressionHumansImmunoblottingMiceMice, KnockoutAnti-Inflammatory Agents, Non-SteroidalAspirinCiliary Neurotrophic FactorCulture Media, ConditionedCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinTumor Necrosis Factor-alphaAstrocytesCell DeathCNTFCREBOligodendrocytesProtein Kinase A (PKA)

Identifiers

PMID23653362
PMCPMC3689994
OpenAlexW2044416158

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.