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      PEP-1-GLRX1 protein exhibits anti-inflammatory effects by inhibiting the activation of MAPK and NF-κB pathways in Raw 264.7 cells

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          Abstract

          Glutaredoxin 1 (GLRX1) has been recognized as an important regulator of redox signaling. Although GLRX1 plays an essential role in cell survival as an antioxidant protein, the function of GLRX1 protein in inflammatory response is still under investigation. Therefore, we wanted to know whether transduced PEP-1-GLRX1 protein inhibits lipopolysaccharide (LPS)- and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced inflammation. In LPS-exposed Raw 264.7 cells, PEP-1-GLRX1 inhibited cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), activation of mitogen activated protein kinases (MAPKs) and nuclear factor-kappaB (NF-βB) expression levels. In a TPA-induced mouse-ear edema model, topically applied PEP-1-GLRX1 transduced into ear tissues and significantly ameliorated ear edema. Our data reveal that PEP-1-GLRX1 attenuates inflammation in vitro and in vivo, suggesting that PEP-1-GLRX1 may be a potential therapeutic protein for inflammatory diseases.

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          Origin and physiological roles of inflammation.

          Ruslan Medzhitov (2008)
          Inflammation underlies a wide variety of physiological and pathological processes. Although the pathological aspects of many types of inflammation are well appreciated, their physiological functions are mostly unknown. The classic instigators of inflammation - infection and tissue injury - are at one end of a large range of adverse conditions that induce inflammation, and they trigger the recruitment of leukocytes and plasma proteins to the affected tissue site. Tissue stress or malfunction similarly induces an adaptive response, which is referred to here as para-inflammation. This response relies mainly on tissue-resident macrophages and is intermediate between the basal homeostatic state and a classic inflammatory response. Para-inflammation is probably responsible for the chronic inflammatory conditions that are associated with modern human diseases.
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            Mitogen-activated protein kinases in innate immunity.

            J. Simon C. Arthur, Steven C Ley (2013)
            Following pathogen infection or tissue damage, the stimulation of pattern recognition receptors on the cell surface and in the cytoplasm of innate immune cells activates members of each of the major mitogen-activated protein kinase (MAPK) subfamilies--the extracellular signal-regulated kinase (ERK), p38 and Jun N-terminal kinase (JNK) subfamilies. In conjunction with the activation of nuclear factor-κB and interferon-regulatory factor transcription factors, MAPK activation induces the expression of multiple genes that together regulate the inflammatory response. In this Review, we discuss our current knowledge about the regulation and the function of MAPKs in innate immunity, as well as the importance of negative feedback loops in limiting MAPK activity to prevent host tissue damage. We also examine how pathogens have evolved complex mechanisms to manipulate MAPK activation to increase their virulence. Finally, we consider the potential of the pharmacological targeting of MAPK pathways to treat autoimmune and inflammatory diseases.
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              Macrophages in inflammation.

              Nagatoshi Fujiwara, Kazuo Kobayashi (2005)
              The inflammatory process is usually tightly regulated, involving both signals that initiate and maintain inflammation and signals that shut the process down. An imbalance between the two signals leaves inflammation unchecked, resulting in cellular and tissue damage. Macrophages are a major component of the mononuclear phagocyte system that consists of closely related cells of bone marrow origin, including blood monocytes, and tissue macrophages. From the blood, monocytes migrate into various tissues and transform macrophages. In inflammation, macrophages have three major function; antigen presentation, phagocytosis, and immunomodulation through production of various cytokines and growth factors. Macrophages play a critical role in the initiation, maintenance, and resolution of inflammation. They are activated and deactivated in the inflammatory process. Activation signals include cytokines (interferon gamma, granulocyte-monocyte colony stimulating factor, and tumor necrosis factor alpha), bacterial lipopolysaccharide, extracellular matrix proteins, and other chemical mediators. Inhibition of inflammation by removal or deactivation of mediators and inflammatory effector cells permits the host to repair damages tissues. Activated macrophages are deactivated by anti-inflammatory cytokines (interleukin 10 and transforming growth factor beta) and cytokine antagonists that are mainly produced by macrophages. Macrophages participate in the autoregulatory loop in the inflammatory process. Because macrophages produce a wide range of biologically active molecules participated in both beneficial and detrimental outcomes in inflammation, therapeutic interventions targeted macrophages and their products may open new avenues for controlling inflammatory diseases.
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                Author and article information

                Journal
                Journal ID (nlm-ta): BMB Rep
                Journal ID (iso-abbrev): BMB Rep
                Title: BMB Reports
                Publisher: Korean Society for Biochemistry and Molecular Biology
                ISSN (Print): 1976-6696
                ISSN (Electronic): 1976-670X
                Publication date (Print): 29 February 2020
                Publication date (Electronic): 29 February 2020
                Publication date PMC-release: 29 February 2020
                Volume: 53
                Issue: 2
                Pages: 106-111
                Affiliations
                [1 ]Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon 24252, Korea
                [2 ]Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangneung-Wonju National University, Gangneung 5457, Korea
                [3 ]Genesen Inc., Seoul 06181, Korea
                [4 ]Department of Green Chemical Engineering, Sangmyung University, Cheonan 31066, Korea
                Author notes
                [* ]Corresponding authors. Soo Young Choi, Tel: +82-33-248-2112; Fax: +82-33-248-3202; E-mail: sychoi@ 123456hallym.ac.kr ; Won Sik Eum, Tel: +82-33-248-3221; Fax: +82-33-248-3202; E-mail: wseum@ 123456hallym.ac.kr
                [#]

                These authors contributed equally to this work.

                Article
                Publisher ID: BMB-53-106
                DOI: 10.5483/BMBRep.2020.53.2.180
                PMC ID: 7061214
                PubMed ID: 31964467
                SO-VID: 85e21723-8c9c-4c92-a722-17ab25403f64
                Copyright © Copyright © 2020 by the The Korean Society for Biochemistry and Molecular Biology
                License:

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

                History
                Date received : 15 July 2019
                Date revision received : 26 July 2019
                Date accepted : 28 August 2019
                Categories
                Subject: Article

                Keywords: inflammation,mapk,nf-βb,pep-1-glrx1,protein therapy
                Data availability:
                Keywords: inflammation, mapk, nf-βb, pep-1-glrx1, protein therapy

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