Evidence map›Paper›PMID 29357041›Full record

ArticleMolecular neurobiology2018

Resolvin D1 Halts Remote Neuroinflammation and Improves Functional Recovery after Focal Brain Damage Via ALX/FPR2 Receptor-Regulated MicroRNAs.

Elisa Bisicchia, Valeria Sasso, Giuseppina Catanzaro, Alessandro Leuti, Zein Mersini Besharat, Martina Chiacchiarini, Marco Molinari, Elisabetta Ferretti, Maria Teresa Viscomi, Valerio Chiurchiù

Abstract read
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Article in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
–field-weighted citation impact
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

68 citing papers in PubMed.

  1. Review
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  13. Omega-3 (Nutrients · 2024
    Review
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  18. Article
  19. Concepts of Regeneration for Spinal Diseases in 2023.International journal of molecular sciences · 2023
    Article
  20. Article

8 more citing papers are in PubMed but not listed here.

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

10 authors.

Elisa BisicchiaIRCCS Santa Lucia Foundation, via del Fosso di Fiorano 64, 00143, Rome, Italy.
Valeria SassoIRCCS Santa Lucia Foundation, via del Fosso di Fiorano 64, 00143, Rome, Italy.
Giuseppina CatanzaroDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Alessandro LeutiIRCCS Santa Lucia Foundation, via del Fosso di Fiorano 64, 00143, Rome, Italy.
Zein Mersini BesharatDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Martina ChiacchiariniDepartment of Molecular Medicine, Sapienza University of Rome, Rome, Italy.
Marco MolinariIRCCS Santa Lucia Foundation, via del Fosso di Fiorano 64, 00143, Rome, Italy.
Elisabetta FerrettiDepartment of Experimental Medicine, Sapienza University of Rome, Rome, Italy.
Maria Teresa ViscomiIRCCS Santa Lucia Foundation, via del Fosso di Fiorano 64, 00143, Rome, Italy. mt.viscomi@hsantalucia.it.ORCID http://orcid.org/0000-0002-9096-4967
Valerio ChiurchiùIRCCS Santa Lucia Foundation, via del Fosso di Fiorano 64, 00143, Rome, Italy. v.chiurchiu@hsantalucia.it.

Funding

Fondazione Italiana Sclerosi Multipla grant 2015/R/8Ministero della Salute GR-2010.2310524
6 · The paper itself

Abstract

Remote damage is a secondary phenomenon that usually occurs after a primary brain damage in regions that are distant, yet functionally connected, and that is critical for determining the outcomes of several CNS pathologies, including traumatic brain and spinal cord injuries. The understanding of remote damage-associated mechanisms has been mostly achieved in several models of focal brain injury such as the hemicerebellectomy (HCb) experimental paradigm, which helped to identify the involvement of many key players, such as inflammation, oxidative stress, apoptosis and autophagy. Currently, few interventions have been shown to successfully limit the progression of secondary damage events and there is still an unmet need for new therapeutic options. Given the emergence of the novel concept of resolution of inflammation, mediated by the newly identified ω3-derived specialized pro-resolving lipid mediators, such as resolvins, we reported a reduced ability of HCb-injured animals to produce resolvin D1 (RvD1) and an increased expression of its target receptor ALX/FPR2 in remote brain regions. The in vivo administration of RvD1 promoted functional recovery and neuroprotection by reducing the activation of Iba-1+ microglia and GFAP+ astrocytes as well as by impairing inflammatory-induced neuronal cell death in remote regions. These effects were counteracted by intracerebroventricular neutralization of ALX/FPR2, whose activation by RvD1 also down-regulated miR-146b- and miR-219a-1-dependent inflammatory markers. In conclusion, we propose that innovative therapies based on RvD1-ALX/FPR2 axis could be exploited to curtail remote damage and enable neuroprotective effects after acute focal brain damage.

Indexed as

Recovery of FunctionAnimalsBrainBrain InjuriesCell DeathCerebellumDocosahexaenoic AcidsDown-RegulationInflammationMaleMicroRNAsNeuronsNeuroprotectionNeuroprotective AgentsRats, WistarReceptors, LipoxinDocosahexaenoic Acidslipoxin A(4) receptor, ratMicroRNAsNeuroprotective AgentsReceptors, Lipoxinresolvin D1EpigeneticsInflammation resolutionNeuroinflammationRemote brain damageSpecialized pro-resolving mediators

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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.