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A Special Class of Messenger Molecules in the Central Nervous...
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A Special Class of Messenger Molecules in the Central Nervous System: The Neuropeptides at the Interplay between Function and Dysfunction

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Clinical Neurology".

Deadline for manuscript submissions: closed (30 September 2019)

Special Issue Editors

Dr. Davide Cervia

E-Mail Website
Guest Editor
Associate Professor of Physiology, Department for Innovation in Biological, Agro-Food and Forest Systems (DIBAF), University of Tuscia, Viterbo, Italy
Interests: neuroprotection; neurodegenerative and neuromuscular disorders; autophagy and apoptosis; signaling mechanisms of cell death/survival; natural compounds; tumor biology
Prof. Dr. Giovanni Casini

E-Mail Website
Guest Editor
Department of Biology, University of Pisa, Pisa, Italy
Interests: neuroprotection; physiology and pathology of the retina; physiology and pathology of the neurovascular unit; regulation of growth factor expression; nutraceuticals
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In the 1970s, an endogenous peptide was found in nerve cells, and the term “neuropeptide” was then introduced. Chemically, neuropeptides have a less complex three-dimensional structure and are smaller than normal proteins, but they are larger than classic neurotransmitters. More than 100 different neuropeptides are currently known to be involved in cell signaling. With some exceptions, almost all peptidergic receptors belong to the superfamily of G-protein-coupled receptors (GPCRs). Commonly, there are several receptor subtypes for a given peptide ligand, and many naturally occurring peptides exhibit a high degree of promiscuity across GPCRs.

After many years of intense research, there is a general agreement that neuropeptides are widely distributed throughout the central nervous system (CNS); they usually act as complementary signals to “classic” neurotransmitters to fine-tune neurotransmission, thereby controlling the balance between excitation and inhibition. In addition, there are well-documented reports of neuropeptides acting as neuroprotectants. Since neuropeptides and their receptors not only are present in neurons and glial cells but also are widely expressed in non-neural cells, neuropeptide functions range from neuromodulators to neuro-hormones, from immune-modulators to growth factors.

The aim of the present Special Issue is to explore and highlight the emerging roles of neuropeptide systems across several functions and dysfunctions of neurons and neural networks. The study of the impact of neuropeptides and their receptors on the pathogenesis of CNS disorders is an area that at present is almost totally unexplored, but, at the same time, may turn out to be extremely important in the design of new therapeutics. We invite authors to contribute with original research at the molecular, cellular, and tissue levels, that will help to better define the contribution of neuropeptides to various aspects of CNS physiopathology. The main goal is to highlight new insights in neuropeptide mechanisms that operate in the brain and that could be involved in human diseases. Reviews that summarize recent findings in both basic and clinical research and discuss current outcomes are also welcome.

Prof. Dr. Davide Cervia
Prof. Dr. Giovanni Casini
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Neuropeptides
  • GPCRs
  • CNS disorders
  • Brain function
  • Brain damage
  • Neuronal signaling
  • Neurotransmission and Neuromodulation
  • Neuroprotection

Published Papers (3 papers)

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Research

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20 pages, 8631 KiB  
Article
New Insights into the Mechanisms of Action of Topical Administration of GLP-1 in an Experimental Model of Diabetic Retinopathy
by Joel Sampedro, Patricia Bogdanov, Hugo Ramos, Cristina Solà-Adell, Mireia Turch, Marta Valeri, Olga Simó-Servat, Carmen Lagunas, Rafael Simó and Cristina Hernández
J. Clin. Med. 2019, 8(3), 339; https://0-doi-org.brum.beds.ac.uk/10.3390/jcm8030339 - 11 Mar 2019
Cited by 35 | Viewed by 4232
Abstract
The main goals of this work were to assess whether the topical administration of glucagon-like peptide-1 (GLP-1) could revert the impairment of the neurovascular unit induced by long-term diabetes (24 weeks) in diabetic mice and to look into the underlying mechanisms. For that [...] Read more.
The main goals of this work were to assess whether the topical administration of glucagon-like peptide-1 (GLP-1) could revert the impairment of the neurovascular unit induced by long-term diabetes (24 weeks) in diabetic mice and to look into the underlying mechanisms. For that reason, db/db mice were treated with eye drops of GLP-1 or vehicle for 3 weeks. Moreover, db/+ mice were used as control. Studies performed in vivo included electroretinogramand the assessment of vascular leakage by using Evans Blue. NF-κB, GFAP and Ki67 proteins were analyzed by immunofluorescence (IF). Additionally, caspase 9, AMPK, IKBα, NF-κB, AKT, GSK3, β-catenin, Bcl-xl, and VEGF were analyzed by WB. Finally, VEGF, IL-1β, IL-6, TNF-α, IL-18, and NLRP3 were studied by reverse transcription-polymerase chain reaction (RT-PCR) and immunofluorescence. We found that topical administration of GLP-1 reverted reactive gliosis and albumin extravasation, and protected against apoptosis and retinal dysfunction. Regarding the involved mechanisms, GLP-1 exerted an anti-inflammatory action by decreasing NF-κB, inflammosome, and pro-inflammatory factors. In addition, it also decreased VEGF expression. Furthermore, GLP-1 promoted cell survival by increasing the anti-apoptotic protein Bcl-xl and the signaling pathway Akt/GSK3b/β-catenin. Finally, Ki67 results revealed that GLP-1 treatment could induce neurogenesis. In conclusion, the topical administration of GLP-1 reverts the impairment of the neurovascular unit by modulating essential pathways involved in the development of diabetic retinopathy (DR). These beneficial effects on the neurovascular unit could pave the way for clinical trials addressed to confirm the effectiveness of GLP-1 in early stages of DR. Full article
(This article belongs to the Special Issue A Special Class of Messenger Molecules in the Central Nervous System: The Neuropeptides at the Interplay between Function and Dysfunction)
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Review

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37 pages, 1007 KiB  
Review
Pituitary Adenylate Cyclase-Activating Polypeptide: 30 Years in Research Spotlight and 600 Million Years in Service
by Viktoria Denes, Peter Geck, Adrienn Mester and Robert Gabriel
J. Clin. Med. 2019, 8(9), 1488; https://0-doi-org.brum.beds.ac.uk/10.3390/jcm8091488 - 18 Sep 2019
Cited by 34 | Viewed by 4516
Abstract
Emerging from the depths of evolution, pituitary adenylate cyclase-activating polypeptide (PACAP) and its receptors (i.e., PAC1, VPAC1, VPAC2) are present in multicellular organisms from Tunicates to humans and govern a remarkable number of physiological processes. Consequently, the clinical relevance of PACAP systems spans [...] Read more.
Emerging from the depths of evolution, pituitary adenylate cyclase-activating polypeptide (PACAP) and its receptors (i.e., PAC1, VPAC1, VPAC2) are present in multicellular organisms from Tunicates to humans and govern a remarkable number of physiological processes. Consequently, the clinical relevance of PACAP systems spans a multifaceted palette that includes more than 40 disorders. We aimed to present the versatility of PACAP1-38 actions with a focus on three aspects: (1) when PACAP1-38 could be a cause of a malfunction, (2) when PACAP1-38 could be the cure for a malfunction, and (3) when PACAP1-38 could either improve or impair biology. PACAP1-38 is implicated in the pathophysiology of migraine and post-traumatic stress disorder whereas an outstanding protective potential has been established in ischemia and in Alzheimer’s disease. Lastly, PACAP receptors could mediate opposing effects both in cancers and in inflammation. In the light of the above, the duration and concentrations of PACAP agents must be carefully set at any application to avoid unwanted consequences. An enormous amount of data accumulated since its discovery (1989) and the first clinical trials are dated in 2017. Thus in the field of PACAP research: “this is not the end, not even the beginning of the end, but maybe the end of the beginning.” Full article
(This article belongs to the Special Issue A Special Class of Messenger Molecules in the Central Nervous System: The Neuropeptides at the Interplay between Function and Dysfunction)
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27 pages, 450 KiB  
Review
Neuroprotective Peptides in Retinal Disease
by Davide Cervia, Elisabetta Catalani and Giovanni Casini
J. Clin. Med. 2019, 8(8), 1146; https://0-doi-org.brum.beds.ac.uk/10.3390/jcm8081146 - 01 Aug 2019
Cited by 26 | Viewed by 3973
Abstract
In the pathogenesis of many disorders, neuronal death plays a key role. It is now assumed that neurodegeneration is caused by multiple and somewhat converging/overlapping death mechanisms, and that neurons are sensitive to unique death styles. In this respect, major advances in the [...] Read more.
In the pathogenesis of many disorders, neuronal death plays a key role. It is now assumed that neurodegeneration is caused by multiple and somewhat converging/overlapping death mechanisms, and that neurons are sensitive to unique death styles. In this respect, major advances in the knowledge of different types, mechanisms, and roles of neurodegeneration are crucial to restore the neuronal functions involved in neuroprotection. Several novel concepts have emerged recently, suggesting that the modulation of the neuropeptide system may provide an entirely new set of pharmacological approaches. Neuropeptides and their receptors are expressed widely in mammalian retinas, where they exert neuromodulatory functions including the processing of visual information. In multiple models of retinal diseases, different peptidergic substances play neuroprotective actions. Herein, we describe the novel advances on the protective roles of neuropeptides in the retina. In particular, we focus on the mechanisms by which peptides affect neuronal death/survival and the vascular lesions commonly associated with retinal neurodegenerative pathologies. The goal is to highlight the therapeutic potential of neuropeptide systems as neuroprotectants in retinal diseases. Full article
(This article belongs to the Special Issue A Special Class of Messenger Molecules in the Central Nervous System: The Neuropeptides at the Interplay between Function and Dysfunction)
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