Microvesicles and exosomes in metabolic diseases and inflammation. (February 2020)

• Record Type: Journal Article
• Authors: Dini, L.; Tacconi, S.; Carata, E.; Tata, A.M.; Vergallo, C.; Panzarini, E.
• Is Part Of: Cytokine & growth factor reviews. Volume 51(2020)
• Page Start: 27
• Page End: 39
• Publication Date: 2020-02
• Subjects: MetS metabolic syndrome -- EVs extracellular vesicles -- T2D type 2 diabetes -- NAFLD non-alcoholic fatty liver disease -- NASH non-alcoholic steatohepatitis -- ATMs adipose tissue macrophages -- TNF-α tumor necrosis factor-alpha -- IL-6 interleukin-6 -- IL-8 inteleukin-8 -- IL-15 inteleukin-15 -- LPS LipoPolySaccharide -- IL-1β inteleukin-1beta -- IFNα interferon alpha -- IFNγ interferon gamma -- CXCL9 chemokine (C-X-C motif) Ligand 9 -- CXCL10 chemokine (C-X-C motif) Ligand 10 -- CXCL11 chemokine (C-X-C motif) Ligand 11 -- IL-4 inteleukin-4 -- TGFβ transforming growth factor beta -- CCL17 chemokine (C-C motif) Ligand 17 -- IL-10 inteleukin-10 -- CD86 cluster of differentiation 86 -- MHC-II major histocompatibility complex class II -- TLR4 toll-like receptor 4 -- CCR7 C-C chemokine receptor type 7 -- CD11c cluster of differentiation 11c -- iNOS inducible NOS -- NF-kB nuclear factor kappa-light-chain-enhancer of activated B cells -- STAT1 signal transducer and activator of transcription 1 -- CD163 cluster of differentiation 163 -- CD206 cluster of differentiation 2016 -- Arg1 arginase 1 -- STAT6 signal transducer and activator of transcription 6 -- WAT white adipose tissue -- CCL3 chemokine (C-C motif) ligand 3 -- DCs dendritic cells -- VAT visceral adipose tissue -- SAT subcutaneous adipose tissue -- G-CSF granulocyte-colony stimulating factor -- NLRP3 NOD-like receptors 3 -- MIP macrophage inflammatory protein -- IR insulin resistance -- IKKβ inhibitor of nuclear factor kappA-B kinase -- JNK1 c-Jun N-terminal kinase -- FFAs free fatty acids -- ROS reactive oxygen species -- AGEs advanced glycation end-products -- AMPK AMP-activated protein kinase -- PBMCs peripheral blood mononuclear cells -- TLRs toll-like receptors family -- UPR unfolded protein response -- DAG diacylglycerol -- FABP fatty acid binding protein activation -- PPAR-γ peroxisome proliferator-activated receptor-γ -- NO nitric oxide -- EXOs exosomes -- MVs microvesicles -- ILVs intraluminal vesicles -- MVBs multivesicular bodies -- ESCRT endosomal sorting complex required for transport -- PS phosphatidylSerine -- Tsg101 tumor susceptibility 101 -- Alix ALG-2 interacting protein X -- HSP heat shock proteins -- miR microRNAs -- LDL low density lipoproteins -- HDL high density lipoproteins -- VLDL very low density lipoproteins -- VEGF vascular endothelial growth factor -- SPRED1 sprouty-related EVH1 domain containing 1 -- ICAM-1 inter-cellular adhesion molecule-1 -- WHO World Health Organization; Metabolic disorders -- Inflammation -- Extracellular vesicles -- M1 macrophages -- M2 macrophages; Cytokines -- Periodicals; 571.84
• DOI: 10.1016/j.cytogfr.2019.12.008
• Languages: English
• ISSNs: 1359-6101

Abstract

Graphical abstract: Highlights: Extracellular vesicles (EVs) are mainly distinguished in exosomes and microvesicles. Recent findings show that EVs are involved in cell-to-cell communication. Both EVs derivation and cargo influence the responsivity of target cells. Macrophage-derived EVs play a key role in MetS-associated inflammation. EVs could be deemed as biomarkers and bioeffectors of metabolic syndrome (MetS). Abstract: Metabolic diseases are based on a dysregulated crosstalk between various cells such as adipocytes, hepatocytes and immune cells. Generally, hormones and metabolites mediate this crosstalk that becomes alterated in metabolic syndrome including obesity and diabetes. Recently, Extracellular Vesicles (EVs) are emerging as a novel way of cell-to-cell communication and represent an attractive strategy to transfer fundamental informations between the cells through the transport of proteins and nucleic acids. EVs, released in the extracellular space, circulate via the various body fluids and modulate the cellular responses following their interaction with the near and far target cells. Clinical and experimental data support their role as biomarkers and bioeffectors in several diseases includimg also the metabolic syndrome. Despite numerous studies on the role of macrophages in the development of metabolic diseases, to date, there are little informations about the influence of metabolic stress on the EVs produced by macrophages and about the role of the released vesicles in the organism. Here, we review current understanding about the role of EVs in metabolic diseases, mainly in inflammation status burst. This knowledge may play a relevant role in health monitoring, medical diagnosis and personalized medicine.