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      Attenuation of Cardiac Ischaemia-reperfusion Injury by Treatment with Hydrogen-rich Water

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          Abstract

          Background: Hydrogen has been shown to exert a bioactive effect on the myocardium. This study examined the signalling pathways for hydrogen attenuating ischaemia-reperfusion injury.

          Methods: In total, 20 male Wistar rats were evaluated for the effects of hydrogen-rich water on ischaemia-reperfusion in hearts. Left ventricular tissue was taken for screening and analysis of active protein factors by protein chip technology. The enrichment of the KEGG pathway was obtained by using the Gene Ontology (GO) enrichment principle. The expression of JAK2, STAT1, STAT3, p-STAT1, p-JAK2, p-STAT3 in rat myocardium was detected by Western blot analysis and immunohistochemistry. The apoptosis rates of the control and hydrogen-rich water groups were detected by TUNEL staining.

          Results: The expression levels of 25 proteins, including five transduction pathways, were downregulated in the hydrogen-rich water group. The expression levels of p-JAK2/JAK2, p-STAT3/STAT3 were upregulated in the hydrogen-rich water group compared with the control group, and p-STAT1/STAT1 was downregulated in the hydrogen-rich water group compared with the control group. Furthermore, the apoptosis rate was significantly decreased in the hydrogen-rich water group, as well.

          Conclusion: Hydrogen-rich water may inhibit the apoptosis of cardiomyocytes after ischaemia-reperfusion by upregulating the expression of the JAK2-STAT3 signalling pathway, which reduces ischaemia-reperfusion injury.

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          Human inflammatory dendritic cells induce Th17 cell differentiation.

          Elodie Segura, Maxime Touzot, Armelle Bohineust … (2013)
          Dendritic cells (DCs) are critical regulators of immune responses. Under noninflammatory conditions, several human DC subsets have been identified. Little is known, however, about the human DC compartment under inflammatory conditions. Here, we characterize a DC population found in human inflammatory fluids that displayed a phenotype distinct from macrophages from the same fluids and from steady-state lymphoid organ and blood DCs. Transcriptome analysis showed that they correspond to a distinct DC subset and share gene signatures with in vitro monocyte-derived DCs. Moreover, human inflammatory DCs, but not inflammatory macrophages, stimulated autologous memory CD4(+) T cells to produce interleukin-17 and induce T helper 17 (Th17) cell differentiation from naive CD4(+) T cells through the selective secretion of Th17 cell-polarizing cytokines. We conclude that inflammatory DCs represent a distinct human DC subset and propose that they are derived from monocytes and are involved in the induction and maintenance of Th17 cell responses. Copyright © 2013 Elsevier Inc. All rights reserved.
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            Regulation of inflammatory responses by IL-17F

            Xuexian O. Yang, Seon Hee Chang, Heon Park … (2008)
            Although interleukin (IL) 17 has been extensively characterized, the function of IL-17F, which has an expression pattern regulated similarly to IL-17, is poorly understood. We show that like IL-17, IL-17F regulates proinflammatory gene expression in vitro, and this requires IL-17 receptor A, tumor necrosis factor receptor–associated factor 6, and Act1. In vivo, overexpression of IL-17F in lung epithelium led to infiltration of lymphocytes and macrophages and mucus hyperplasia, similar to observations made in IL-17 transgenic mice. To further understand the function of IL-17F, we generated and analyzed mice deficient in IL-17F or IL-17. IL-17, but not IL-17F, was required for the initiation of experimental autoimmune encephalomyelitis. Mice deficient in IL-17F, but not IL-17, had defective airway neutrophilia in response to allergen challenge. Moreover, in an asthma model, although IL-17 deficiency reduced T helper type 2 responses, IL-17F–deficient mice displayed enhanced type 2 cytokine production and eosinophil function. In addition, IL-17F deficiency resulted in reduced colitis caused by dextran sulfate sodium, whereas IL-17 knockout mice developed more severe disease. Our results thus demonstrate that IL-17F is an important regulator of inflammatory responses that seems to function differently than IL-17 in immune responses and diseases.
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              FMS-like tyrosine kinase 3 is required for dendritic cell development in peripheral lymphoid tissues

              Claudia Waskow, Kang Liu, Guillaume Darrasse-Jèze … (2008)
              Dendritic cell (DC) development begins in the bone marrow but is not completed until after immature progenitors reach their sites of residence in lymphoid organs. The hematopoietic growth factors regulating these processes are poorly understood. Here we examine the effects of FMS-like tyrosine kinase 3 (Flt3) signaling on macrophage DC progenitors (MDP) in the bone marrow and on peripheral DCs. We find that the MDP compartment is responsive to super–physiologic levels of Flt3 ligand (Flt3L) but is not dependent on Flt3 for its homeostatic maintenance in vivo. In contrast, Flt3 is essential in regulation of homeostatic DC development in the spleen where it is required to maintain normal numbers of DCs by controlling their division in the periphery.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Curr Mol Med
                Journal ID (iso-abbrev): Curr. Mol. Med
                Journal ID (publisher-id): CMM
                Title: Current Molecular Medicine
                Publisher: Bentham Science Publishers
                ISSN (Print): 1566-5240
                ISSN (Electronic): 1875-5666
                Publication date (Electronic): May 2019
                Publication date (Print): May 2019
                Volume: 19
                Issue: 4
                Pages: 294-302
                Affiliations
                School of Medicine, Hebei University , Baoding , 071000 , China;

                School of Chemistry, Hebei University , Baoding , 071000 , China;

                Centre for Cardiovascular Biology and Atherosclerosis Research, Division of Cardiovascular Medicine, Department of Internal Medicine, University of Texas Medical School at Houston , Houston, , TX, 77030 ;

                Department of Cardiac Surgery, Affiliated Hospital of Hebei University , Baoding , 071000 , China
                Author notes
                [# ]Address correspondence to this author at the School of Medicine, Hebei University, Baoding 071000, China; E-mails: lful666@ 123456sina.com and zyj@ 123456hbu.edu.cn
                [*]

                These authors contributed equally to this work.

                Article
                Publisher ID: CMM-19-294
                DOI: 10.2174/1566524019666190321113544
                PMC ID: 7061975
                PubMed ID: 30907314
                SO-VID: 143bc848-6c91-4e31-b260-f084656e00df
                Copyright © © 2019 Bentham Science Publishers
                License:

                This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/legalcode), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited.

                History
                Date received : 30 December 2018
                Date revision received : 18 February 2019
                Date accepted : 19 March 2019
                Categories
                Subject: Article

                ScienceOpen disciplines: Molecular medicine
                Keywords: hydrogen-rich water,ischaemia-reperfusion injury,jak-stat signalling pathway,protein chip technique,apoptosis
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: hydrogen-rich water, ischaemia-reperfusion injury, jak-stat signalling pathway, protein chip technique, apoptosis

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