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      The emerging role of Toll-like receptor 4 in myocardial inflammation

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          Abstract

          Toll-like receptors (TLRs) are a family of pattern recognition receptors involved in cardiovascular diseases. Notably, numerous studies have demonstrated that TLR4 activates the expression of several of pro-inflammatory cytokine genes that play pivotal roles in myocardial inflammation, particularly myocarditis, myocardial infarction, ischemia-reperfusion injury, and heart failure. In addition, TLR4 is an emerging target for anti-inflammatory therapies. Given the significance of TLR4, it would be useful to summarize the current literature on the molecular mechanisms and roles of TLR4 in myocardial inflammation. Thus, in this review, we first introduce the basic knowledge of the TLR4 gene and describe the activation and signaling pathways of TLR4 in myocardial inflammation. Moreover, we highlight the recent progress of research on the involvement of TLR4 in myocardial inflammation. The information reviewed here may be useful to further experimental research and to increase the potential of TLR4 as a therapeutic target.

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          Assembly and localization of Toll-like receptor signalling complexes.

          Nicholas J. Gay, Martyn Symmons, Monique Gangloff … (2014)
          Signal transduction by the Toll-like receptors (TLRs) is central to host defence against many pathogenic microorganisms and also underlies a large burden of human disease. Thus, the mechanisms and regulation of signalling by TLRs are of considerable interest. In this Review, we discuss the molecular basis for the recognition of pathogen-associated molecular patterns, the nature of the protein complexes that mediate signalling, and the way in which signals are regulated and integrated at the level of allosteric assembly, post-translational modification and subcellular trafficking of the components of the signalling complexes. These fundamental molecular mechanisms determine whether the signalling output leads to a protective immune response or to serious pathologies such as sepsis. A detailed understanding of these processes at the molecular level provides a rational framework for the development of new drugs that can specifically target pathological rather than protective signalling in inflammatory and autoimmune disease.
          Article 0 comments Cited 298 times – based on 0 reviews     Review now
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            Inflammation, immunity, and hypertensive end-organ damage.

            William G McMaster, Annet Kirabo, Meena S Madhur … (2015)
            For >50 years, it has been recognized that immunity contributes to hypertension. Recent data have defined an important role of T cells and various T cell-derived cytokines in several models of experimental hypertension. These studies have shown that stimuli like angiotensin II, deoxycorticosterone acetate-salt, and excessive catecholamines lead to formation of effector like T cells that infiltrate the kidney and perivascular regions of both large arteries and arterioles. There is also accumulation of monocyte/macrophages in these regions. Cytokines released from these cells, including interleukin-17, interferon-γ, tumor necrosis factorα, and interleukin-6 promote both renal and vascular dysfunction and damage, leading to enhanced sodium retention and increased systemic vascular resistance. The renal effects of these cytokines remain to be fully defined, but include enhanced formation of angiotensinogen, increased sodium reabsorption, and increased renal fibrosis. Recent experiments have defined a link between oxidative stress and immune activation in hypertension. These have shown that hypertension is associated with formation of reactive oxygen species in dendritic cells that lead to formation of gamma ketoaldehydes, or isoketals. These rapidly adduct to protein lysines and are presented by dendritic cells as neoantigens that activate T cells and promote hypertension. Thus, cells of both the innate and adaptive immune system contribute to end-organ damage and dysfunction in hypertension. Therapeutic interventions to reduce activation of these cells may prove beneficial in reducing end-organ damage and preventing consequences of hypertension, including myocardial infarction, heart failure, renal failure, and stroke.
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              Discrimination of bacterial lipoproteins by Toll-like receptor 6.

              O Takeuchi, T Kawai, P F Mühlradt … (2001)
              Bacterial lipoproteins (BLP) trigger immune responses via Toll-like receptor 2 (TLR2) and their immunostimulatory properties are attributed to the presence of a lipoylated N-terminus. Most BLP are triacylated at the N-terminus cysteine residue, but mycoplasmal macrophage-activating lipopeptide-2 kD (MALP-2) is only diacylated. Here we show that TLR6-deficient (TLR6(-/-)) cells are unresponsive to MALP-2 but retain their normal responses to lipopeptides of other bacterial origins. Reconstitution experiments in TLR2(-/-) TLR6(-/-) embryonic fibroblasts reveal that co-expression of TLR2 and TLR6 is absolutely required for MALP-2 responsiveness. Taken together, these results show that TLR6 recognizes MALP-2 cooperatively with TLR2, and appears to discriminate between the N-terminal lipoylated structures of MALP-2 and lipopeptides derived from other bacteria.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cell Death Dis
                Journal ID (iso-abbrev): Cell Death Dis
                Title: Cell Death & Disease
                Publisher: Nature Publishing Group
                ISSN (Electronic): 2041-4889
                Publication date (Print): May 2016
                Publication date (Electronic): 26 May 2016
                Publication date PMC-release: 1 May 2016
                Volume: 7
                Issue: 5
                Page: e2234
                Affiliations
                [1 ]Department of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University , 127 Changle West Road, Xi'an 710032, China
                [2 ]Department of Thoracic and Cardiovascular Surgery, Affiliated Drum Tower Hospital of Nanjing University Medical School , 321 Zhongshan Road, Nanjing, Jiangsu 210008, China
                [3 ]Department of Biomedical Engineering, The Fourth Military Medical University , 169 Changle West Road, Xi'an 710032, China
                [4 ]Department of Aerospace Medicine, The Fourth Military Medical University , Xi'an 710032, China
                [5 ]Department of Thoracic Surgery, Tangdu Hospital, The Fourth Military Medical University , 1 Xinsi Road, Xi'an 710038, China
                [6 ]Department of Geriatrics, Xijing Hospital, The Fourth Military Medical University , 127 Changle West Road, Xi'an 710032, China
                Author notes
                [* ]Department of Cardiovascular Surgery, Xijing Hospital, The Fourth Military Medical University , 127 Changle West Road, Xi'an 710032, China. Tel: +86 29 84775314; Fax: +86 29 83210092; E-mail: yiweifmmu@ 123456126.com or yangsun111@ 123456126.com
                [7]

                These authors contributed equally to this work.

                Article
                Publisher Item ID: cddis2016140
                DOI: 10.1038/cddis.2016.140
                PMC ID: 4917669
                PubMed ID: 27228349
                SO-VID: 5e7ea9a1-219b-466a-b500-b3ded119b65b
                Copyright © Copyright © 2016 Macmillan Publishers Limited
                License:

                Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

                History
                Date received : 02 January 2016
                Date revision received : 25 March 2016
                Date accepted : 12 April 2016
                Categories
                Subject: Review

                ScienceOpen disciplines: Cell biology
                Data availability:
                ScienceOpen disciplines: Cell biology

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