Evidence map›Paper›PMID 33072073›Full record

ArticleFrontiers in immunology2020

Prokineticin Receptor Inhibition With PC1 Protects Mouse Primary Sensory Neurons From Neurotoxic Effects of Chemotherapeutic Drugs

Giorgia Moschetti, Theodora Kalpachidou, Giada Amodeo, Roberta Lattanzi, Paola Sacerdote, Michaela Kress, Silvia Franchi

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing 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

10 citing papers in PubMed, 15 citations in OpenAlex.

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  8. Article
  9. Article
  10. Pathological Mechanisms of Bortezomib-Induced Peripheral Neuropathy.International journal of molecular sciences · 2021
    Review
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 4 institutions in 2 countries.

Giorgia MoschettiDepartment of Pharmacological and Biomolecular Sciences, Università Degli Studi di Milano, Milan, Italy.
Theodora KalpachidouDepartment of Physiology and Biomedical Physics, Medical University of Innsbruck, Innsbruck, Austria.
Giada AmodeoDepartment of Pharmacological and Biomolecular Sciences, Università Degli Studi di Milano, Milan, Italy.
Roberta LattanziDepartment of Physiology and Pharmacology "Vittorio Erspamer", Sapienza University of Rome, Rome, Italy.
Paola SacerdoteDepartment of Pharmacological and Biomolecular Sciences, Università Degli Studi di Milano, Milan, Italy.
Michaela KressDepartment of Physiology and Biomedical Physics, Medical University of Innsbruck, Innsbruck, Austria.
Silvia FranchiDepartment of Pharmacological and Biomolecular Sciences, Università Degli Studi di Milano, Milan, Italy.
University of Milan · ITInnsbruck Medical University · ATSapienza University of Rome · ITUniversität Innsbruck · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurotoxicity is a common side effect of chemotherapeutics that often leads to the development of chemotherapy-induced peripheral neuropathy (CIPN). The peptide Prokineticin 2 (PK2) has a key role in experimental models of CIPN and can be considered an insult-inducible endangering mediator. Since primary afferent sensory neurons are highly sensitive to anticancer drugs, giving rise to dysesthesias, the aim of our study was to evaluate the alterations induced by vincristine (VCR) and bortezomib (BTZ) exposure in sensory neuron cultures and the possible preventive effect of blocking PK2 signaling. Both VCR and BTZ induced a concentration-dependent reduction of total neurite length that was prevented by the PK receptor antagonist PC1. Antagonizing the PK system also reduced the upregulation of PK2, PK-R1, TLR4, IL-6, and IL-10 expression induced by chemotherapeutic drugs. In conclusion, inhibition of PK signaling with PC1 prevented the neurotoxic effects of chemotherapeutics, suggesting a promising strategy for neuroprotective therapies against the sensory neuron damage induced by exposure to these drugs.

Indexed as

AnimalsAntineoplastic AgentsBortezomibCells, CulturedDose-Response Relationship, DrugDown-RegulationDrug Evaluation, PreclinicalGastrointestinal HormonesGene Expression RegulationMaleMiceMice, Inbred C57BLNerve Tissue ProteinsNeuritesNeuroimmunomodulationNeuropeptidesAntineoplastic AgentsBortezomibGastrointestinal HormonesNerve Tissue ProteinsNeuropeptidesNeuroprotective AgentsProk2 protein, mouseRNA, MessengerTriazinesVincristinechemotherapyDRGneuronsneurotoxicityprokineticins

Identifiers

PMID33072073
PMCPMC7541916
OpenAlexW3089000170

What OpenQuestion holds

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Registered trials

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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.