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7 results on '"Marconi, V."'

1. The prokineticin receptor antagonist PC1 rescues memory impairment induced by β amyloid administration through the modulation of prokineticin system.

Author

Maftei D, Ratano P, Fusco I, Marconi V, Squillace S, Negri L, Severini C, Balboni G, Steardo L, Bronzuoli MR, Scuderi C, Campolongo P, and Lattanzi R

Subjects
Amyloid beta-Peptides toxicity, Animals, Disease Models, Animal, Gastrointestinal Hormones genetics, Gastrointestinal Hormones metabolism, Gliosis, Guanidines pharmacology, Hippocampus metabolism, Infusions, Intraventricular, Male, Maze Learning, Memory drug effects, NF-kappa B drug effects, NF-kappa B metabolism, Neurogenesis drug effects, Neuropeptides genetics, Neuropeptides metabolism, Nitric Oxide Synthase Type II drug effects, Nitric Oxide Synthase Type II metabolism, Peptide Fragments toxicity, Rats, Receptors, G-Protein-Coupled genetics, Receptors, G-Protein-Coupled metabolism, Receptors, Peptide genetics, Receptors, Peptide metabolism, Reverse Transcriptase Polymerase Chain Reaction, Spatial Learning drug effects, Triazines pharmacology, Alzheimer Disease, Hippocampus drug effects, Learning drug effects, Neuropeptides drug effects, Neuroprotective Agents pharmacology, Receptors, G-Protein-Coupled antagonists & inhibitors, Receptors, Peptide antagonists & inhibitors
Abstract

Growing evidences demonstrate that chemokines and chemokine receptors are up-regulated in resident central nervous system cells during Alzheimer's disease contributing to neuroinflammation and neurodegeneration. Prokineticin 2 belongs to a new family of chemokines which recently emerged as a critical player in immune system and inflammatory diseases. Since pharmacological blockade in vitro of the prokineticin system is able to antagonize Amyloid β-induced neurotoxicity, the aim of the present study was to investigate in vivo effects of prokineticin receptor antagonist PC1 on memory impairment in a rodent model of Alzheimer's disease. Rats were intracerebroventricular infused with Aβ 1-42 and behavioral responses as well as the expression profile in hippocampus of prokineticin 2 and its receptors were investigated. Results demonstrated that Aβ 1-42 -infused rats developed significant memory impairments together with a marked up-regulation of both prokineticin 2 and its receptors in hippocampal neurons and astrocytes. Treatment with PC1 significantly improved learning capability of Aβ 1-42 -infused rats restoring the balance of prokineticin system. This study pointed to a neuroprotective role of PC1 on Aβ 1-42 -induced memory deficits that could be ascribed to the ability of PC1 to modulate rat hippocampal prokineticin system and to recover the impaired Aβ 1-42 -induced neurogenesis. This suggests that prokineticin system antagonism could be considered as a new approach for the study of AD etiopathology., (Copyright © 2019. Published by Elsevier Ltd.)

Published
2019
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2. Bv8/prokineticin 2 is involved in Aβ-induced neurotoxicity.

Author

Severini C, Lattanzi R, Maftei D, Marconi V, Ciotti MT, Petrocchi Passeri P, Florenzano F, Del Duca E, Caioli S, Zona C, Balboni G, Salvadori S, Nisticò R, and Negri L

Subjects
Alzheimer Disease genetics, Alzheimer Disease metabolism, Amyloid beta-Peptides toxicity, Animals, Apoptosis drug effects, Gastrointestinal Hormones genetics, Gene Expression Regulation drug effects, Hippocampus metabolism, Long-Term Potentiation drug effects, Long-Term Potentiation genetics, Male, Mice, Mice, Transgenic, Neurons drug effects, Neuropeptides genetics, Peptide Fragments metabolism, Peptide Fragments toxicity, Protein Transport, Rats, Receptors, G-Protein-Coupled antagonists & inhibitors, Receptors, G-Protein-Coupled genetics, Receptors, G-Protein-Coupled metabolism, Up-Regulation, Amyloid beta-Peptides metabolism, Gastrointestinal Hormones metabolism, Neurons metabolism, Neuropeptides metabolism
Abstract

Bv8/Prokineticin 2 (PROK2) is a bioactive peptide initially discovered as a regulator of gastrointestinal motility. Among multiple biological roles demonstrated for PROK2, it was recently established that PROK2 is an insult-inducible endangering mediator for cerebral damage. Aim of the present study was to evaluate the PROK2 and its receptors' potential involvement in amyloid beta (Aβ) neurotoxicity, a hallmark of Alzheimer's disease (AD) and various forms of traumatic brain injury (TBI). Analyzing primary cortical cultures (CNs) and cortex and hippocampus from Aβ treated rats, we found that PROK2 and its receptors PKR1 and PKR2 mRNA are up-regulated by Aβ, suggesting their potential involvement in AD. Hence we evaluated if impairing the prokineticin system activation might have protective effect against neuronal death induced by Aβ. We found that a PKR antagonist concentration-dependently protects CNs against Aβ(1-42)-induced neurotoxicity, by reducing the Aβ-induced PROK2 neuronal up-regulation. Moreover, the antagonist completely rescued LTP impairment in hippocampal slices from 6 month-old Tg2576 AD mice without affecting basal synaptic transmission and paired pulse-facilitation paradigms. These results indicate that PROK2 plays a role in cerebral amyloidosis and that PROK2 antagonists may represent a new approach for ameliorating the defining pathology of AD.

Published
2015
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3. Prokineticin 2 upregulation in the peripheral nervous system has a major role in triggering and maintaining neuropathic pain in the chronic constriction injury model.

Author

Lattanzi R, Maftei D, Marconi V, Florenzano F, Franchi S, Borsani E, Rodella LF, Balboni G, Salvadori S, Sacerdote P, and Negri L

Subjects
Animals, Macrophages metabolism, Macrophages pathology, Male, Mice, Neuralgia pathology, Receptors, G-Protein-Coupled metabolism, Schwann Cells pathology, Sciatic Nerve injuries, Sciatic Nerve pathology, Subtilisins metabolism, Gastrointestinal Hormones biosynthesis, Neuralgia metabolism, Neuropeptides biosynthesis, Schwann Cells metabolism, Sciatic Nerve metabolism, Signal Transduction, Up-Regulation
Abstract

The new chemokine Prokineticin 2 (PROK2) and its receptors (PKR1 and PKR2) have a role in inflammatory pain and immunomodulation. Here we identified PROK2 as a critical mediator of neuropathic pain in the chronic constriction injury (CCI) of the sciatic nerve in mice and demonstrated that blocking the prokineticin receptors with two PKR1-preferring antagonists (PC1 and PC7) reduces pain and nerve damage. PROK2 mRNA expression was upregulated in the injured nerve since day 3 post injury (dpi) and in the ipsilateral DRG since 6 dpi. PROK2 protein overexpression was evident in Schwann Cells, infiltrating macrophages and axons in the peripheral nerve and in the neuronal bodies and some satellite cells in the DRG. Therapeutic treatment of neuropathic mice with the PKR-antagonist, PC1, impaired the PROK2 upregulation and signalling. This fact, besides alleviating pain, brought down the burden of proinflammatory cytokines in the damaged nerve and prompted an anti-inflammatory repair program. Such a treatment also reduced intraneural oedema and axon degeneration as demonstrated by the physiological skin innervation and thickness conserved in CCI-PC1 mice. These findings suggest that PROK2 plays a crucial role in neuropathic pain and might represent a novel target of treatment for this disease.

Published
2015
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4. PC1, a non-peptide PKR1-preferring antagonist, reduces pain behavior and spinal neuronal sensitization in neuropathic mice.

Author

Guida F, Lattanzi R, Boccella S, Maftei D, Romano R, Marconi V, Balboni G, Salvadori S, Scafuro MA, de Novellis V, Negri L, Maione S, and Luongo L

Subjects
Animals, Astrocytes drug effects, Astrocytes metabolism, Behavior, Animal drug effects, Gastrointestinal Hormones genetics, Hot Temperature, Hyperalgesia drug therapy, Hyperalgesia metabolism, Male, Mice, Neuralgia metabolism, Neurons drug effects, Neurons physiology, Neuropeptides genetics, Peripheral Nerve Injuries drug therapy, Peripheral Nerve Injuries metabolism, RNA, Messenger metabolism, Receptors, G-Protein-Coupled genetics, Receptors, G-Protein-Coupled metabolism, Sciatic Nerve drug effects, Sciatic Nerve injuries, Sciatic Nerve metabolism, Spinal Cord metabolism, Spinal Cord physiology, Triazines pharmacology, Analgesics therapeutic use, Gastrointestinal Hormones metabolism, Neuralgia drug therapy, Neuropeptides metabolism, Receptors, G-Protein-Coupled antagonists & inhibitors, Spinal Cord drug effects, Triazines therapeutic use
Abstract

Peripheral neuropathy is characterized by abnormal pain responses triggered by the release of several mediators and neuronal hyperexcitability at the spinal cord level. Emerging evidence indicates that the enhanced activity of dorsal horn neurons requires communication with glia and microglia, cells that are physiologically involved in neuronal wellbeing. Prokineticins (PKs), which include PK1 and PK2, represent a novel family of chemokines characterized by a unique structural motif comprising five disulfide bonds. They are expressed in the peripheral and central nervous system. PKs bind two G protein coupled receptors, PKR1 and PKR2, and participate in the regulation of several biological processes, including pain sensation. This study aimed to investigate the anti-nociceptive effect of PC1, a non-peptide PKR1-preferring antagonist, in a mouse model of neuropathic pain. To do this, we assessed the activity of spinal cord nociceptive neurons as well as astrocyte and microglia phenotypes after repeated administration of PC1 in vivo. PC1 treatment strongly delayed the development of thermal hyperalgesia and tactile and mechanical allodynia. It also reduced spinal microglial and glial activation 8 days post injury in spared nerve injury (SNI) mice. Neuropathic mice showed an increased level of PK2 protein in the spinal cord, mostly in astrocytes. PC1 treatment completely reversed the increased responsiveness to mechanical stimuli, the decreased threshold of neuronal activation, and the increased spontaneous activity that were observed in nociceptive specific (NS) neurons of SNI mice., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

Published
2015
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5. Controlling the activation of the Bv8/prokineticin system reduces neuroinflammation and abolishes thermal and tactile hyperalgesia in neuropathic animals.

Author

Maftei D, Marconi V, Florenzano F, Giancotti LA, Castelli M, Moretti S, Borsani E, Rodella LF, Balboni G, Luongo L, Maione S, Sacerdote P, Negri L, and Lattanzi R

Subjects
Animals, Ganglia, Spinal metabolism, Gastrointestinal Hormones genetics, Hyperalgesia drug therapy, Interleukin-10 genetics, Interleukin-10 metabolism, Interleukin-1beta genetics, Interleukin-1beta metabolism, Male, Mice, Neuralgia drug therapy, Neuroglia metabolism, Neuropeptides genetics, RNA, Messenger metabolism, Receptors, G-Protein-Coupled antagonists & inhibitors, Receptors, G-Protein-Coupled genetics, Sciatic Nerve metabolism, Spinal Cord metabolism, Gastrointestinal Hormones metabolism, Hyperalgesia metabolism, Neuralgia metabolism, Neuropeptides metabolism, Receptors, G-Protein-Coupled metabolism
Abstract

Background and Purpose: Chemokines are involved in neuroinflammation and contribute to chronic pain processing. The new chemokine prokineticin 2 (PROK2) and its receptors (PKR1 and PKR2 ) have a role in inflammatory pain and immunomodulation. In the present study, we investigated the involvement of PROK2 and its receptors in neuropathic pain., Experimental Approach: Effects of single, intrathecal, perineural and s.c. injections of the PKR antagonist PC1, or of 1 week s.c. treatment, on thermal hyperalgesia and tactile allodynia was evaluated in mice with chronic constriction of the sciatic nerve (CCI). Expression and localization of PROK2 and of its receptors at peripheral and central level was evaluated 10 days after CCI, following treatment for 1 week with saline or PC1. IL-1β and IL-10 levels, along with glia activation, were evaluated., Key Results: Subcutaneous, intrathecal and perineural PC1 acutely abolished the CCI-induced hyperalgesia and allodynia. At 10 days after CCI, PROK2 and its receptor PKR2 were up-regulated in nociceptors, in Schwann cells and in activated astrocytes of the spinal cord. Therapeutic treatment with PC1 (s.c., 1 week) alleviated established thermal hyperalgesia and allodynia, reduced the injury-induced overexpression of PROK2, significantly blunted nerve injury-induced microgliosis and astrocyte activation in the spinal cord and restored the physiological levels of proinflammatory and anti-inflammatory cytokines in periphery and in spinal cord., Conclusion and Implications: The prokineticin system contributes to pain modulation via neuron-glia interaction. Sustained inhibition of the prokineticin system, at peripheral or central levels, blocked both pain symptoms and some events underlying disease progression., (© 2014 The British Pharmacological Society.)

Published
2014
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6. PC1, a non-peptide PKR1-preferring antagonist, reduces pain behavior and spinal neuronal sensitization in neuropathic mice

Author

De Novellis, Ma Scafuro, Daniela Maftei, Livio Luongo, S. Salvadori, Serena Boccella, Gianfranco Balboni, Francesca Guida, Roberta Lattanzi, Marconi, Lucia Negri, Sabatino Maione, Rosaria Romano, Guida, Francesca, Lattanzi, R, Boccella, S, Maftei, D, Romano, Rosa Lucia, Marconi, V, Balboni, G, Salvadori, S, Scafuro, Ma, DE NOVELLIS, Vito, Negri, L, Maione, Sabatino, and Luongo, Livio

Subjects
Male, Hot Temperature, Messenger, Neuropathic pain, Receptors, G-Protein-Coupled, Mice, Peripheral Nerve Injuries, Receptors, Neurons, Gastrointestinal Hormone, Analgesics, Spinal cord, Behavior, Animal, Triazines, Medicine (all), Sciatic Nerve, Electrophysiology, Triazine, Nociception, medicine.anatomical_structure, Hyperalgesia, Microglia, medicine.symptom, Astrocyte, SNi, Central nervous system, Glia, Prokineticin system, Animals, Astrocytes, Gastrointestinal Hormones, Neuralgia, Neuropeptides, RNA, Messenger, Spinal Cord, Pharmacology, NO, G-Protein-Coupled, medicine, Behavior, Animal, business.industry, Peripheral Nerve Injurie, Neuron, Nerve injury, Neuropeptide, nervous system, RNA, Analgesic, business, Neuroscience
Abstract

Peripheral neuropathy is characterized by abnormal pain responses triggered by the release of several mediators and neuronal hyperexcitability at the spinal cord level. Emerging evidence indicates that the enhanced activity of dorsal horn neurons requires communication with glia and microglia, cells that are physiologically involved in neuronal wellbeing. Prokineticins (PKs), which include PK1 and PK2, represent a novel family of chemokines characterized by a unique structural motif comprising five disulfide bonds. They are expressed in the peripheral and central nervous system. PKs bind two G protein coupled receptors, PKR1 and PKR2, and participate in the regulation of several biological processes, including pain sensation. This study aimed to investigate the anti-nociceptive effect of PC1, a non-peptide PKR1-preferring antagonist, in a mouse model of neuropathic pain. To do this, we assessed the activity of spinal cord nociceptive neurons as well as astrocyte and microglia phenotypes after repeated administration of PC1 in vivo. PC1 treatment strongly delayed the development of thermal hyperalgesia and tactile and mechanical allodynia. It also reduced spinal microglial and glial activation 8 days post injury in spared nerve injury (SNI) mice. Neuropathic mice showed an increased level of PK2 protein in the spinal cord, mostly in astrocytes. PC1 treatment completely reversed the increased responsiveness to mechanical stimuli, the decreased threshold of neuronal activation, and the increased spontaneous activity that were observed in nociceptive specific (NS) neurons of SNI mice.

Published
2015

7. Controlling the activation of the Bv8/prokineticin system reduces neuroinflammation and abolishes thermal and tactile hyperalgesia in neuropathic animals

Author

Maftei, Daniela, Marconi, Veronica, Florenzano, F, Giancotti, La, Castelli, M, Moretti, S, Borsani, E, Rodella, Lf, Balboni, G, Luongo, L, Maione, S, Sacerdote, P, Negri, L, Lattanzi, Roberta, Maftei, D., Marconi, V., Florenzano, F., Giancotti, L. A., Castelli, M., Moretti, S., Borsani, E., Rodella, L. F., Balboni, G., Luongo, L., Maione, S., Sacerdote, P., Negri, L., and Lattanzi, R.

Subjects
Male, Interleukin-1beta, Neuropeptides, Research Papers, Sciatic Nerve, Interleukin-10, Receptors, G-Protein-Coupled, Gastrointestinal Hormones, Mice, prokineticin, Spinal Cord, pain, bv8, Hyperalgesia, Ganglia, Spinal, Animals, Neuralgia, RNA, Messenger, Neuroglia
Abstract

Chemokines are involved in neuroinflammation and contribute to chronic pain processing. The new chemokine prokineticin 2 (PROK2) and its receptors (PKR1 and PKR2 ) have a role in inflammatory pain and immunomodulation. In the present study, we investigated the involvement of PROK2 and its receptors in neuropathic pain.Effects of single, intrathecal, perineural and s.c. injections of the PKR antagonist PC1, or of 1 week s.c. treatment, on thermal hyperalgesia and tactile allodynia was evaluated in mice with chronic constriction of the sciatic nerve (CCI). Expression and localization of PROK2 and of its receptors at peripheral and central level was evaluated 10 days after CCI, following treatment for 1 week with saline or PC1. IL-1β and IL-10 levels, along with glia activation, were evaluated.Subcutaneous, intrathecal and perineural PC1 acutely abolished the CCI-induced hyperalgesia and allodynia. At 10 days after CCI, PROK2 and its receptor PKR2 were up-regulated in nociceptors, in Schwann cells and in activated astrocytes of the spinal cord. Therapeutic treatment with PC1 (s.c., 1 week) alleviated established thermal hyperalgesia and allodynia, reduced the injury-induced overexpression of PROK2, significantly blunted nerve injury-induced microgliosis and astrocyte activation in the spinal cord and restored the physiological levels of proinflammatory and anti-inflammatory cytokines in periphery and in spinal cord.The prokineticin system contributes to pain modulation via neuron-glia interaction. Sustained inhibition of the prokineticin system, at peripheral or central levels, blocked both pain symptoms and some events underlying disease progression.

Published
2014

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