Evidence map›Paper›PMID 18607779›Full record

ArticleJournal of molecular neuroscience : MN2008

Agonistic behavior of PACAP6-38 on sensory nerve terminals and cytotrophoblast cells.

D Reglodi, R Borzsei, T Bagoly, A Boronkai, B Racz, A Tamas, P Kiss, G Horvath, R Brubel, J Nemeth and 2 more

Abstract read
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In one paragraph

Article in Journal of molecular neuroscience : MN, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 38% 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

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Effects of Pituitary Adenylate Cyclase Activating Polypeptide on Cell Death.International journal of molecular sciences · 2022
    Review
  4. Article
  5. Review
  6. Article
  7. Protective Effects of PACAP in Peripheral Organs.Frontiers in endocrinology · 2020
    Review
  8. PACAP38 and PACThe journal of headache and pain · 2018
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. 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

12 authors at 3 institutions in 1 country.

D ReglodiDepartment of Anatomy, University of Pecs, Pecs, Hungary.
R Borzsei
T Bagoly
A Boronkai
B Racz
A Tamas
P Kiss
G Horvath
R Brubel
J Nemeth
G Toth
Z Helyes
University of Pecs · HUUniversity of Debrecen · HUUniversity of Szeged · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The effects of pituitary adenylate cyclase activating polypeptide (PACAP) are mediated through G-protein-coupled receptors, the specific PAC1 receptor and VPAC1 and VPAC2 receptors which bind vasoactive intestinal peptide with similar affinity. Based on binding affinity studies, PACAP6-38 was discovered as a potent antagonist of PAC1 and it has been used by hundreds of studies as a PACAP antagonist. Recently, we have found that in certain cells/tissues, PACAP6-38 does not antagonize PACAP-induced effects, but surprisingly, it exerts similar actions to PACAP1-38, behaving as an agonist. In the present study, we report on the agonistic behavior of PACAP6-38 on neuropeptide release from sensory nerves of the isolated rat trachea and on the MAPK signaling pathways in cytotrophoblast cells. In isolated rat tracheae, PACAP6-38, similarly to PACAP1-38, induced significant inhibitory effects on the release of three simultaneously measured sensory neuropeptides, substance P, calcitonin gene-related peptide, and somatostatin evoked by both chemical excitation and electrical field stimulation of capsaicin-sensitive afferents. Effects of PACAP6-38 were the same as those of PACAP1-38 on MAPK signaling in human cytotrophoblast cells. Western blot analysis showed that both peptide forms stimulated ERK1/2 and JNK phosphorylation, while they both inhibited p38 MAPK phosphorylation. The most pronounced effects were observed when both peptides were present. In summary, our results show that PACAP6-38, which is a PACAP receptor antagonist in most cells/tissues, can behave as an agonist in other systems. The increasing interest in the effects of PACAP requires further studies on the pharmacological properties of the peptide and its analogues.

Indexed as

TrophoblastsAnimalsCalcitonin Gene-Related PeptideCapsaicinCell Line, TumorHumansMaleMAP Kinase Signaling SystemMitogen-Activated Protein KinasesPeptide FragmentsPituitary Adenylate Cyclase-Activating PolypeptideRatsRats, WistarSensory Receptor CellsSensory System AgentsSomatostatinCalcitonin Gene-Related PeptideCapsaicinMitogen-Activated Protein KinasesPeptide Fragmentspituitary adenylate-cyclase-activating-peptide (6-38)Pituitary Adenylate Cyclase-Activating PolypeptideSensory System AgentsSomatostatinSubstance P

Identifiers

PMID18607779
OpenAlexW1966995878

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.