For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
14
views
35
references
 Top references
cited by
11
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      319
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Tat-ATOX1 inhibits inflammatory responses via regulation of MAPK and NF-κB pathways

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          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

          Antioxidant 1 (ATOX1) protein has been reported to exhibit various protective functions, including antioxidant and chaperone. However, the effects of ATOX1 on the inflammatory response has not been fully elucidated. Thus, we prepared cell permeable Tat-ATOX1 and studied the effects on lipopolysaccharide (LPS)- and 12-O-tetradecanoyl phorbol-13-acetate (TPA)-induced inflammation. Experimental results showed that transduced Tat-ATOX1 protein significantly suppressed LPS-induced intracellular reactive oxygen species (ROS). Also, Tat-ATOX1 protein markedly inhibited LPS- and TPA-induced inflammatory responses by decreasing cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) and further inhibited phosphorylation of mitogen activated protein kinases (MAPKs; JNK, ERK and p38) and the nuclear factor-kappaB (NF-κB) signaling pathway. These results indicate that the Tat-ATOX1 protein has a pivotal role in inflammation via inhibition of inflammatory responses, suggesting Tat-ATOX1 protein may offer a therapeutic strategy for inflammation.

          Related collections

          Most cited references35

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

          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.
          Article 0 comments Cited 1846 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The inflammasomes: guardians of the body.

            Fabio Martinon, Annick Mayor, Jurg Tschopp (2009)
            The innate immune system relies on its capacity to rapidly detect invading pathogenic microbes as foreign and to eliminate them. The discovery of Toll-like receptors (TLRs) provided a class of membrane receptors that sense extracellular microbes and trigger antipathogen signaling cascades. More recently, intracellular microbial sensors have been identified, including NOD-like receptors (NLRs). Some of the NLRs also sense nonmicrobial danger signals and form large cytoplasmic complexes called inflammasomes that link the sensing of microbial products and metabolic stress to the proteolytic activation of the proinflammatory cytokines IL-1beta and IL-18. The NALP3 inflammasome has been associated with several autoinflammatory conditions including gout. Likewise, the NALP3 inflammasome is a crucial element in the adjuvant effect of aluminum and can direct a humoral adaptive immune response. In this review, we discuss the role of NLRs, and in particular the inflammasomes, in the recognition of microbial and danger components and the role they play in health and disease.
            Article 0 comments Cited 688 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Macrophages and tissue injury: agents of defense or destruction?

              Jeffrey D. Laskin, Jessica C. Gardner, Debra L. Laskin … (2010)
              The past several years have seen the accumulation of evidence demonstrating that tissue injury induced by diverse toxicants is due not only to their direct effects on target tissues but also indirectly to the actions of resident and infiltrating macrophages. These cells release an array of mediators with cytotoxic, pro- and anti-inflammatory, angiogenic, fibrogenic, and mitogenic activity, which function to fight infections, limit tissue injury, and promote wound healing. However, following exposure to toxicants, macrophages can become hyperresponsive, resulting in uncontrolled or dysregulated release of mediators that exacerbate acute tissue injury and/or promote the development of chronic diseases such as fibrosis and cancer. Evidence suggests that the diverse activity of macrophages is mediated by distinct subpopulations that develop in response to signals within their microenvironment. Understanding the precise roles of these different macrophage populations in the pathogenic response to toxicants is key to designing effective treatments for minimizing tissue damage and chronic disease and for facilitating wound repair.
              Article 0 comments Cited 185 times – based on 0 reviews     Review now
                Bookmark
                All references

                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): December 2018
                Publication date (Electronic): 31 December 2018
                Volume: 51
                Issue: 12
                Pages: 654-659
                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 25457, Korea
                [3 ]R&D Center, Lumieye Genetics Co., Ltd., Seoul 06198, 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-51-654
                DOI: 10.5483/BMBRep.2018.51.12.248
                PMC ID: 6330941
                PubMed ID: 30545441
                SO-VID: 7f7ada4c-8387-4e30-8052-8bb378041ea1
                Copyright © Copyright © 2018 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 : 26 October 2018
                Date revision received : 09 November 2018
                Date accepted : 21 November 2018
                Categories
                Subject: Articles

                Keywords: inflammation,mapk,nf-κb,protein therapy,tat-atox1
                Data availability:
                Keywords: inflammation, mapk, nf-κb, protein therapy, tat-atox1

                Comments

                Comment on this article

                scite_

                Similar content319

                See all similar

                Cited by11

                See all cited by

                Most referenced authors672

                See all reference authors