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Cells
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Cholinergic Signaling in Brain Disease
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Cholinergic Signaling in Brain Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cell Signaling".

Deadline for manuscript submissions: closed (1 December 2021) | Viewed by 6764

Special Issue Editor

Dr. Nadine Kabbani

E-Mail Website
Guest Editor
School of Systems Biology, George Mason University, Fairfax, VA 22030, USA
Interests: evolution; cell signaling; neuroscience; science policy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Acetylcholine is amongst the most primitive of chemical transmitters for cell-to-cell communication in both plants and animals. By binding to its cognate cell-surface metabotropic and ionotropic receptors, acetylcholine (cholinergic) has evolved to regulate, through its signaling, vital physiological processes in mammals including cognition, endocrine and vascular control, and reproduction. From early research on the neuromuscular synapse to the isolation and structural study of the nicotinic acetylcholine receptor, studies have unraveled the critical and, at times nuanced, molecular mechanisms of cholinergic signaling in immune, epithelial, neural, and other cell types. Disruptions of cholinergic production and signaling are now recognized features in devasting and often costly human diseases and conditions. These include various forms of cancer, schizophrenia, Alzheimer’s disease, and adaptive as well as acquired immune conditions. 

This Special Issue will provide a timely collection of research on and insights into the mechanisms of cholinergic signaling and regulation within cells. Building on knowledge gained from molecular biology, electrophysiology, proteomic and bioinformatic analysis, and a wide range of genetic tools and cellular probes, this Special Issue will gather trends and highlight emergent findings in the mechanisms and pathways of cholinergic signaling and regulation across cell types. Of particular interest are processes implicated in the pathophysiology of Alzheimer’s disease, addiction, cancer, immunity, pain, vascular and cardiac function, neurodevelopment, and degeneration. Additionally, insights and findings in mechanistic pathways of epigenetic modification and gene-environment interaction are highly welcome, as are discoveries on therapeutic interventions through cholinergic targeting.  

I look forward to your contribution.

Dr. Nadine Kabbani
Guest Editor

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. Cells 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 2700 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

  • Neurodegeneration
  • Synaptic Plasticity
  • Receptor Signaling
  • Cholinergic Transmission
  • Cancer
  • Nicotine

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Published Papers (2 papers)

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Research

14 pages, 4464 KiB  
Article
Mitochondrial Disruption by Amyloid Beta 42 Identified by Proteomics and Pathway Mapping
by Patricia Sinclair, Ancha Baranova and Nadine Kabbani
Cells 2021, 10(9), 2380; https://doi.org/10.3390/cells10092380 - 10 Sep 2021
Cited by 13 | Viewed by 2966
Abstract
Alzheimer’s disease (AD) is marked by chronic neurodegeneration associated with the occurrence of plaques containing amyloid β (Aβ) proteins in various parts of the human brain. An increase in several Aβ fragments is well documented in patients with AD and anti-amyloid targeting is [...] Read more.
Alzheimer’s disease (AD) is marked by chronic neurodegeneration associated with the occurrence of plaques containing amyloid β (Aβ) proteins in various parts of the human brain. An increase in several Aβ fragments is well documented in patients with AD and anti-amyloid targeting is an emerging area of therapy. Soluble Aβ can bind to various cell surface and intracellular molecules with the pathogenic Aβ42 fragment leading to neurotoxicity. Here we examined the effect of Aβ42 on network adaptations in the proteome of nerve growth factor (NGF) differentiated PC12 cells using liquid-chromatography electrospray ionization mass spectrometry (LC-ESI MS/MS) proteomics. Whole-cell peptide mass fingerprinting was coupled to bioinformatic gene set enrichment analysis (GSEA) in order to identify differentially represented proteins and related gene ontology (GO) pathways within Aβ42 treated cells. Our results underscore a role for Aβ42 in disrupting proteome responses for signaling, bioenergetics, and morphology in mitochondria. These findings highlight the specific components of the mitochondrial response during Aβ42 neurotoxicity and suggest several new biomarkers for detection and surveillance of amyloid disease. Full article
(This article belongs to the Special Issue Cholinergic Signaling in Brain Disease)
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8 pages, 1172 KiB  
Article
Apigenin and Structurally Related Flavonoids Allosterically Potentiate the Function of Human α7-Nicotinic Acetylcholine Receptors Expressed in SH-EP1 Cells
by Waheed Shabbir, Keun-Hang Susan Yang, Bassem Sadek and Murat Oz
Cells 2021, 10(5), 1110; https://doi.org/10.3390/cells10051110 - 5 May 2021
Cited by 8 | Viewed by 3226
Abstract
Phytochemicals, such as monoterpenes, polyphenols, curcuminoids, and flavonoids, are known to have anti-inflammatory, antioxidant, neuroprotective, and procognitive effects. In this study, the effects of several polyhydroxy flavonoids, as derivatives of differently substituted 5,7-dihydroxy-4H-chromen-4-one including apigenin, genistein, luteolin, kaempferol, quercetin, gossypetin, and [...] Read more.
Phytochemicals, such as monoterpenes, polyphenols, curcuminoids, and flavonoids, are known to have anti-inflammatory, antioxidant, neuroprotective, and procognitive effects. In this study, the effects of several polyhydroxy flavonoids, as derivatives of differently substituted 5,7-dihydroxy-4H-chromen-4-one including apigenin, genistein, luteolin, kaempferol, quercetin, gossypetin, and phloretin with different lipophilicities (cLogP), as well as topological polar surface area (TPSA), were tested for induction of Ca2+ transients by α7 human nicotinic acetylcholine (α7 nACh) receptors expressed in SH-EP1 cells. Apigenin (10 μM) caused a significant potentiation of ACh (30 μM)-induced Ca2+ transients, but did not affect Ca2+ transients induced by high K+ (60 mM) containing solutions. Co-application of apigenin with ACh was equally effective as apigenin preincubation. However, the effect of apigenin significantly diminished by increasing ACh concentrations. The flavonoids tested also potentiated α7 nACh mediated Ca2+ transients with descending potency (highest to lowest) by genistein, gossypetin, kaempferol, luteolin, phloretin, quercetin, and apigenin. The specific binding of α7 nACh receptor antagonist [125I]-bungarotoxin remained unchanged in the presence of any of the tested polyhydroxy flavonoids, suggesting that these compounds act as positive allosteric modulators of the α7-nACh receptor in SH-EP1 cells. These findings suggest a clinical potential for these phytochemicals in the treatment of various human diseases from pain to inflammation and neural disease. Full article
(This article belongs to the Special Issue Cholinergic Signaling in Brain Disease)
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