Evidence map›Paper›PMID 23869659›Full record

ArticleBritish journal of pharmacology2013

Comparative assessment of PDE 4 and 7 inhibitors as therapeutic agents in experimental autoimmune encephalomyelitis.

C González-García, B Bravo, A Ballester, R Gómez-Pérez, C Eguiluz, M Redondo, A Martínez, C Gil, S Ballester

Open access · greenAbstract readComparative Study
In one paragraph

Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing 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

25 citing papers in PubMed, 52 citations in OpenAlex.

  1. Review
  2. Article
  3. PDE4D: A Multipurpose Pharmacological Target.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. The Role of PDE8 in T Cell Recruitment and Function in Inflammation.Frontiers in cell and developmental biology · 2021
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
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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

9 authors at 3 institutions in 1 country.

C González-GarcíaUnidad de Regulación Génica, UFIEC, Instituto de Salud Carlos III, Madrid, Spain.
B Bravo
A Ballester
R Gómez-Pérez
C Eguiluz
M Redondo
A Martínez
C Gil
S Ballester
Unidad Funcional de Investigación de Enfermedades Crónicas · ESInstituto de Química Médica · ESInstituto de Salud Carlos III · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposePDE4 inhibition suppresses experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). However, side effects hinder PDE4 inhibitors clinical use. PDE7 inhibition might constitute an alternative therapeutic strategy, but few data about the anti-inflammatory potential of PDE7 inhibitors are currently available. We have used the EAE model to perform a comparative evaluation of PDE4 and PDE7 inhibition as strategies for MS treatment. EXPERIMENTAL APPROACH: Two PDE7 inhibitors, the sulfonamide derivative BRL50481 and the recently described quinazoline compound TC3.6, were assayed to modulate EAE in SJL mice, in comparison with the well-known PDE4 inhibitor Rolipram. We evaluated clinical signs, presence of inflammatory infiltrates in CNS and anti-inflammatory markers. We also analysed the effect of these inhibitors on the inflammatory profile of spleen cells in vitro. KEY

resultsTC3.6 prevented EAE with efficacy similar to Rolipram, while BRL50481 had no effect on the disease. Differences between both PDE7 inhibitors are discussed. Data from Rolipram and TC3.6 showed that PDE4 and PDE7 inhibition work through both common and distinct pathways. Rolipram administration caused an increase in IL-10 and IL-27 expression which was not found after TC3.6 treatment. On the other hand, both inhibitors reduced IL-17 levels, prevented infiltration in CNS and increased the expression of the T regulator cell marker Foxp3. CONCLUSIONS AND IMPLICATIONS: These results provide new information about the effects of Rolipram on EAE, underline PDE7 inhibition as a new therapeutic target for inflammatory diseases and show the value of TC3.6 to prevent EAE, with possible consequences for new therapeutic tools in MS.

Indexed as

AnimalsAnti-Inflammatory AgentsBrainCells, CulturedCyclic Nucleotide Phosphodiesterases, Type 4Cyclic Nucleotide Phosphodiesterases, Type 7Encephalomyelitis, Autoimmune, ExperimentalForkhead Transcription FactorsInflammation MediatorsInterleukin-10Interleukin-17InterleukinsMiceMice, Inbred C57BLPhosphodiesterase 4 InhibitorsRolipramAnti-Inflammatory AgentsCyclic Nucleotide Phosphodiesterases, Type 4Cyclic Nucleotide Phosphodiesterases, Type 7Forkhead Transcription FactorsFoxp3 protein, mouseIL10 protein, mouseIl27 protein, mouseInflammation MediatorsInterleukin-10Interleukin-17InterleukinsPhosphodiesterase 4 InhibitorsRolipramEAEinflammationinhibitorPDE

Identifiers

PMID23869659
PMCPMC3791998
OpenAlexW1560855374

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.