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Cholinergic Signaling in Human Health and Diseases 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (30 March 2022) | Viewed by 2559

Special Issue Editor


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Guest Editor
Suntory Foundation for Life Sciences, Bioorganic Research Institute, Kyoto 619-0284, Japan
Interests: intestinal organoid; stem cell; signaling; non-neuronal acetylcholine; acetylcholine receptor
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of our previous Special Issue "Cholinergic Signaling in Human Health and Diseases".

It is now well-established that acetylcholine (ACh) and its receptors (nicotinic and muscarinic receptors (n- and mAChRs)) as important constituents of the cholinergic system are ubiquitous molecules in life. Other components of the cholinergic system (choline acetyltransferase (ChAT), choline transporter (ChT), and acetylcholinesterase (AChE)) have also been demonstrated in mammalian non-neuronal cells, including those of humans. The traditional view of ACh regards it as a neurotransmitter. In addition to neurotransmission, ACh plays important roles in various aspects of cell biology and homeostasis outside of the nervous system. ACh is actually synthesized by all live cells and plays an intermediary role in the interactions of non-neuronal cells with the external environment, endocrine hormones, growth factors, cytokines, and the central nervous system. Thus, cholinergic signaling in non-neuronal cells is comparable to neuronal cholinergic signaling. In addition to improving our understanding of the structure and function of the cholinergic system, significant progress has also been made in elucidating the roles of neuronal and non-neuronal ACh in the pathogenesis and treatment of human disease. This Issue will explore new insights into how cholinergic signaling functions in mammals, how its roles contribute to protecting the body from disease, and how the molecules can be manipulated to treat disease.

Dr. Toshio Takahashi
Guest Editor

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Keywords

  • neuron
  • immune cell
  • stem cell
  • signaling
  • acetylcholine (ACh)
  • non-neuronal ACh
  • acetylcholine receptor
  • acetylcholine receptor to muscarinic ACh receptor
  • nicotinic ACh receptor

Published Papers (1 paper)

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Research

8 pages, 851 KiB  
Communication
Expression and Function of Nicotinic Acetylcholine Receptors in Induced Regulatory T Cells
by Yuichiro Nakata, Kento Miura, Norimasa Yamasaki, Sawako Ogata, Shuka Miura, Naohisa Hosomi and Osamu Kaminuma
Int. J. Mol. Sci. 2022, 23(3), 1779; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23031779 - 04 Feb 2022
Cited by 7 | Viewed by 1922
Abstract
A contribution of the cholinergic system to immune cell function has been suggested, though the role of nicotine and its receptors in T cells, especially regulatory T (Treg) cells, is unclear. We herein investigated the expression and function of nicotinic acetylcholine receptors (nAChRs) [...] Read more.
A contribution of the cholinergic system to immune cell function has been suggested, though the role of nicotine and its receptors in T cells, especially regulatory T (Treg) cells, is unclear. We herein investigated the expression and function of nicotinic acetylcholine receptors (nAChRs) in murine-induced Treg (iTreg) cells. Upon differentiation of naive BALB/c T cells into iTreg cells and other T-cell subsets, the effect of nicotine on cytokine production and proliferation of iTreg cells was examined. The expression of nAChRs and its regulatory mechanisms were comparatively analyzed among T-cell subsets. Stimulation-induced transforming growth factor-β1 (TGF-β1) production of iTreg cells was suppressed by nicotine, whereas interleukin (IL)-10 production and proliferation was not affected. α2-, α5-, α9-, and β2-nAChRs were differentially expressed in naive, Th1, Th2, Th9, Th17, and iTreg cells. Among these cell types, the α9-nAChR was particularly upregulated in iTreg cells via its gene promoter, but not through tri-methylation at the 4th lysine residue of the histone H3-dependent mechanisms. We conclude that the immunoregulatory role of Treg cells is modified by the cholinergic system, probably through the characteristic expression of nAChRs. Full article
(This article belongs to the Special Issue Cholinergic Signaling in Human Health and Diseases 2.0)
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