Evidence map›Paper›PMID 34638592›Full record

ArticleInternational journal of molecular sciences2021

The Antagonism of the Prokineticin System Counteracts Bortezomib Induced Side Effects: Focus on Mood Alterations.

Giada Amodeo, Benedetta Verduci, Patrizia Sartori, Patrizia Procacci, Vincenzo Conte, Gianfranco Balboni, Paola Sacerdote, Silvia Franchi

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Giada AmodeoDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Vanvitelli 32, 20129 Milan, Italy.ORCID 0000-0002-4097-3195
Benedetta VerduciDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Vanvitelli 32, 20129 Milan, Italy.
Patrizia SartoriDepartment of Biomedical Sciences for Health, Università degli Studi di Milano, Via Colombo 71, 20133 Milan, Italy.ORCID 0000-0002-4806-2337
Patrizia ProcacciDepartment of Biomedical Sciences for Health, Università degli Studi di Milano, Via Colombo 71, 20133 Milan, Italy.ORCID 0000-0003-4726-2115
Vincenzo ConteDepartment of Biomedical Sciences for Health, Università degli Studi di Milano, Via Colombo 71, 20133 Milan, Italy.
Gianfranco BalboniDepartment of Life and Environmental Sciences, University of Cagliari, Via Ospedale 72, 09124 Cagliari, Italy.ORCID 0000-0003-4437-6096
Paola SacerdoteDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Vanvitelli 32, 20129 Milan, Italy.
Silvia FranchiDepartment of Pharmacological and Biomolecular Sciences, Università degli Studi di Milano, Via Vanvitelli 32, 20129 Milan, Italy.
University of Milan · ITUniversity of Cagliari · IT

Funding

Fondazione Cariplo 2015-0897
6 · The paper itself

Abstract

The development of neuropathy and of mood alterations is frequent after chemotherapy. These complications, independent from the antitumoral mechanism, are interconnected due to an overlapping in their processing pathways and a common neuroinflammatory condition. This study aims to verify whether in mice the treatment with the proteasome inhibitor bortezomib (BTZ), at a protocol capable of inducing painful neuropathy, is associated with anxiety, depression and supraspinal neuroinflammation. We also verify if the therapeutic treatment with the antagonist of the prokineticin (PK) system PC1, which is known to contrast pain and neuroinflammation, can prevent mood alterations. Mice were treated with BTZ (0.4 mg/kg three times/week for 4 weeks); mechanical allodynia and locomotor activity were evaluated over time while anxiety (dark light and marble burying test), depression (sucrose preference and swimming test) and supraspinal neuroinflammation were checked at the end of the protocol. BTZ treated neuropathic mice develop anxiety and depression. The presence of mood alterations is related to the presence of neuroinflammation and PK system activation in prefrontal cortex, hippocampus and hypothalamus with high levels of PK2 and PKR2 receptor, IL-6 and TNF-α, TLR4 and an upregulation of glial markers. PC1 treatment, counteracting pain, prevented the development of supraspinal inflammation and depression-like behavior in BTZ mice.

Indexed as

AffectAnimalsAnxietyBiomarkersBortezomibCytokinesDepressionDisease Models, AnimalHippocampusHyperalgesiaHypothalamusInflammationLocomotionMaleMiceMice, Inbred C57BLBiomarkersBortezomibCytokinesProteasome InhibitorsReceptors, G-Protein-CoupledVascular Endothelial Growth Factor, Endocrine-Gland-Derivedanxietychemotherapy-induced side effectsdepressionneuroinflammationneuropathic painprokineticin system

Identifiers

PMID34638592
PMCPMC8508359
OpenAlexW3199282764

What OpenQuestion holds

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LicenceCC BY
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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.