3
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Signaling pathway mechanisms of neurological diseases induced by G protein‐coupled receptor 39

      review-article
      1 , 1 , , 1 ,
      CNS Neuroscience & Therapeutics
      John Wiley and Sons Inc.
      GPR39, GPR39 agonist, GPR39 signaling, zinc

      Read this article at

          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          G protein‐coupled receptor 39 (GPR39) is a transmembrane zinc receptor with two splice variants, which belongs to the G‐protein‐coupled receptor growth hormone‐releasing peptide family. Its expression is induced by zinc, which activates GPR39, and its activation mediates cell proliferation, ion homeostasis, and anti‐inflammatory, antioxidant, and other pathophysiological effects via different signaling pathways.

          Aims

          The article reviews the latest literature in this field. In particular, the role of GPR39 in nervous system is discussed.

          Materials and methods

          GPR39 can be a promising target in neurological diseases for targeted therapy, which will help doctors overcome the associated problems.

          Discussion

          GPR39 is expressed in vivo at several sites. Increasing evidence suggests that GPR39 plays an important role as a neuroprotective agent in vivo and regulates various neurological functions, including neurodegeneration, neuroelectrophysiology, and neurovascular homeostasis.

          Conclusion

          This review aims to provide an overview of the functions, signal transduction pathways, and pathophysiological role of GPR39 in neurological diseases and summarize the GPR39 agonists that have been identified in the recent years.

          Abstract

          The expression of G protein‐coupled receptor 39 (GPR39) is induced by zinc, which activates GPR39 and later mediates cell proliferation, ion homeostasis maintenance, anti‐inflammatory, antioxidant, and other pathophysiological effects through different signaling pathways. It plays an important neuroprotective role in neurodegeneration, neuroelectrophysiology, and neurovascular homeostasis.

          Related collections

          Most cited references104

          • Record: found
          • Abstract: found
          • Article: not found

          Multiple sclerosis - a review

          Multiple sclerosis (MS) is the commonest non-traumatic disabling disease to affect young adults. The incidence of MS is increasing worldwide, together with the socioeconomic impact of the disease. The underlying cause of MS and mechanisms behind this increase remain opaque, although complex gene-environment interactions almost certainly play a significant role. The epidemiology of MS indicates that low serum levels of vitamin D, smoking, childhood obesity and infection with the Epstein-Barr virus are likely to play a role in disease development. Changes in diagnostic methods and criteria mean that people with MS can be diagnosed increasingly early in their disease trajectory. Alongside this, treatments for MS have increased exponentially in number, efficacy and risk. There is now the possibility of a diagnosis of 'pre-symptomatic MS' being made; as a result potentially preventive strategies could be studied. In this comprehensive review, MS epidemiology, potential aetiological factors and pathology are discussed, before moving on to clinical aspects of MS diagnosis and management.
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Neurobiology of BDNF in fear memory, sensitivity to stress, and stress-related disorders

              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              GPR39 signaling is stimulated by zinc ions but not by obestatin.

              GPR39 is an orphan member of the ghrelin receptor family that recently was suggested to be the receptor for obestatin, a peptide derived from the ghrelin precursor. Here, we compare the effect of obestatin to the effect of Zn(2+) on signal transduction and study the effect of obestatin on food intake. Although Zn(2+) stimulated inositol phosphate turnover, cAMP production, arrestin mobilization, as well as cAMP response element-dependent and serum response element-dependent transcriptional activity in GPR39-expressing cells as opposed to mock-transfected cells, no reproducible effect was obtained with obestatin in the GPR39-expressing cells. Moreover, no specific binding of obestatin could be detected in two different types of GPR39-expressing cells using three different radioiodinated forms of obestatin. By quantitative PCR analysis, GPR39 expression was readily detected in peripheral organs such as duodenum and kidney but not in the pituitary and hypothalamus, i.e. presumed central target organs for obestatin. Obestatin had no significant and reproducible effect on acute food intake in either freely fed or fasted lean mice. It is concluded that GPR39 is probably not the obestatin receptor. In contrast, the potency and efficacy of Zn(2+) in respect of activating signaling indicates that this metal ion could be a physiologically relevant agonist or modulator of GPR39.
                Bookmark

                Author and article information

                Contributors
                wjw_999@126.com
                fengjuan99999@hotmail.com
                Journal
                CNS Neurosci Ther
                CNS Neurosci Ther
                10.1111/(ISSN)1755-5949
                CNS
                CNS Neuroscience & Therapeutics
                John Wiley and Sons Inc. (Hoboken )
                1755-5930
                1755-5949
                21 March 2023
                June 2023
                : 29
                : 6 ( doiID: 10.1002/cns.v29.6 )
                : 1470-1483
                Affiliations
                [ 1 ] Department of Neurology Shengjing Hospital of China Medical University Shenyang China
                Author notes
                [*] [* ] Correspondence

                Jue Wang and Juan Feng Department of Neurology, Shengjing Hospital of China Medical University, 36 Sanhao St, Shenyang 110004, China.

                Email: wjw_999@ 123456126.com and fengjuan99999@ 123456hotmail.com

                Author information
                https://orcid.org/0000-0002-4902-8915
                Article
                CNS14174 CNSNT-2022-1012.R1
                10.1111/cns.14174
                10173710
                36942516
                d2195188-1edb-4b41-be78-c9e0101bf319
                © 2023 The Authors. CNS Neuroscience & Therapeutics published by John Wiley & Sons Ltd.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 14 February 2023
                : 21 November 2022
                : 28 February 2023
                Page count
                Figures: 4, Tables: 0, Pages: 14, Words: 10693
                Funding
                Funded by: National Natural Science Foundation of China , doi 10.13039/501100001809;
                Award ID: 82271275
                Award ID: 82271353
                Funded by: Outstanding Scientific Fund of Shengjing Hospital
                Categories
                Review
                Reviews
                Custom metadata
                2.0
                June 2023
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.2.8 mode:remove_FC converted:11.05.2023

                Neurosciences
                gpr39,gpr39 agonist,gpr39 signaling,zinc
                Neurosciences
                gpr39, gpr39 agonist, gpr39 signaling, zinc

                Comments

                Comment on this article