Editorial: Role of Macrophage MicroRNAs in Inflammatory Diseases and Cancer.
Ontology highlight
ABSTRACT:
SUBMITTER: Renaudineau Y
PROVIDER: S-EPMC8477417 | biostudies-literature | 2021
REPOSITORIES: biostudies-literature
Publications
Editorial: Role of Macrophage MicroRNAs in Inflammatory Diseases and Cancer.
Renaudineau Yves Y Berindan-Neagoe Ioana I Stanciu Luminita Aurelia LA
Frontiers in immunology 20210913
Similar Datasets
Project description: Not available
| S-EPMC10951382 | biostudies-literature
Project description:The etiopathogenesis of autoimmune skin diseases is complex and still not fully understood. The role of epigenetic factors is emphasized in the development of such diseases. MicroRNAs (miRNAs), a group of non-coding RNAs (ncRNAs-non-coding RNAs), are one of the important post-transcriptional epigenetic factors. miRNAs have a significant role in the regulation of the immune response by participating in the process of the differentiation and activation of B and T lymphocytes, macrophages, and dendritic cells. Recent advances in research on epigenetic factors have provided new insights into the pathogenesis and potential diagnostic and therapeutic targets of many pathologies. Numerous studies revealed a change in the expression of some microRNAs in inflammatory skin disorders, and the regulation of miRNA expression is a promising therapeutic goal. This review presents the state of the art regarding changes in the expression and role of miRNAs in inflammatory and autoimmune skin diseases, including psoriasis, atopic dermatitis, vitiligo, lichen planus, hidradenitis suppurativa, and autoimmune blistering diseases.
| S-EPMC10253000 | biostudies-literature
Project description:Inflammation is a complicated biological and pathophysiological cascade of responses to infections and injuries, and inflammatory mechanisms are closely related to many diseases. The magnitude, the complicated network of pro- and anti-inflammatory factors, and the direction of the inflammatory response can impact on the development and progression of various disorders. The currently available treatment strategies often target the symptoms and not the causes of inflammatory disease and may often be ineffective. Since the onset and termination of inflammation are crucial to prevent tissue damage, a range of mechanisms has evolved in nature to regulate the process including negative and positive feedback loops. In this regard, microRNAs (miRNAs) have emerged as key gene regulators to control inflammation, and it is speculated that they are fine-tune signaling regulators to allow for proper resolution and prevent uncontrolled progress of inflammatory reactions. In this review, we discuss recent findings related to significant roles of miRNAs in immune regulation, especially the potential utility of these molecules as novel anti-inflammatory agents to treat inflammatory diseases. Furthermore, we discuss the possibilities of using miRNAs as drugs in the form of miRNA mimics or miRNA antagonists.
| S-EPMC6026627 | biostudies-literature
Project description:MicroRNAs (miRNAs, miRs) are short, endogenously initiated, non-coding RNAs that bind to target mRNAs, leading to the degradation or translational suppression of respective mRNAs. They have been reported as key players in physiological processes like differentiation, cellular proliferation, development, and apoptosis. They have gained importance as gene expression regulators in the immune system. They control antibody production and release various inflammatory mediators. Abnormal expression and functioning of miRNA in the immune system is linked to various diseases like inflammatory disorders, allergic diseases, cancers etc. As compared to the average human genome, miRNA targets the genes of immune system quite differently. miRNA appeared to regulate the responses related to both acquired and innate immunity of the humans. Several miRNAs importantly regulate the transcription and even, dysregulation of inflammation-related mediators. Many miRNAs are either upregulated or downregulated in various inflammatory and infectious diseases. Hence, modifying or targeting the expression of miRNAs might serve as a novel strategy for the diagnosis, prevention, and treatment of various inflammatory and infectious conditions.
| S-EPMC6992578 | biostudies-literature
Project description: Not available
| S-EPMC10703367 | biostudies-literature
Project description: Not available
| S-EPMC6650930 | biostudies-literature
Project description:Chemokines are a large family of small secreted proteins that have fundamental roles in organ development, normal physiology, and immune responses upon binding to their corresponding receptors. The primary functions of chemokines are to coordinate and recruit immune cells to and from tissues and to participate in regulating interactions between immune cells. In addition to the generally recognized antimicrobial immunity, the chemokine/chemokine receptor axis also exerts a tumorigenic function in many different cancer models and is involved in the formation of immunosuppressive and protective tumor microenvironment (TME), making them potential prognostic markers for various hematologic and solid tumors. In fact, apart from its vital role in tumors, almost all inflammatory diseases involve chemokines and their receptors in one way or another. Modulating the expression of chemokines and/or their corresponding receptors on tumor cells or immune cells provides the basis for the exploitation of new drugs for clinical evaluation in the treatment of related diseases. Here, we summarize recent advances of chemokine systems in protumor and antitumor immune responses and discuss the prevailing understanding of how the chemokine system operates in inflammatory diseases. In this review, we also emphatically highlight the complexity of the chemokine system and explore its potential to guide the treatment of cancer and inflammatory diseases.
| S-EPMC9175564 | biostudies-literature
Project description:Inflammatory arthritis including rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA) exhibit the shared feature of changes in activation and polarization of circulating monocytes and tissue macrophages. Numerous microRNAs (miRs) have been found to have key functions in regulating inflammation and macrophage polarization. Although there is increasing interest in the roles of miRs in both RA and JIA, less is known regarding how miRs relate to functional properties of immune cells, including monocytes and macrophages. Interestingly, miRs can function both to promote inflammatory phenotypes and pro-inflammatory polarization, as well as through negative-feedback loops to limit inflammation. Here, we review the functional roles of several miRs in macrophages in inflammatory arthritis, with a particular focus on vivo effects of miR alteration in experimental arthritis. We also consider how current efforts to target miRs clinically could modify functional monocyte and macrophage polarization in vivo, and serve as novel therapies for diseases such as RA and JIA.
| S-EPMC6753331 | biostudies-literature
Project description:MicroRNAs (miRNAs) represent a class of small non-coding RNAs that control gene expression by targeting messenger RNA (mRNA). Recently, it has been demonstrated that miRNA expression is altered in many human diseases including cancers, suggesting that miRNA may play a potential role in the pathogenesis of different diseases. It has also been reported that there is a unique expression pattern of miRNAs in the disease state differing from the normal state. In this review, we focus on the miRNA signatures in different human diseases including cancers. Such signatures may be used as diagnostic and prognostic markers.
| S-EPMC2744658 | biostudies-other
Project description:Macrophages are mononuclear phagocytes which derive either from blood-borne monocytes or reside as resident macrophages in peripheral (Kupffer cells of the liver, marginal zone macrophages of the spleen, alveolar macrophages of the lung) and central tissue (microglia). They occur as M1 (pro-inflammatory; classic) or M2 (anti-inflammatory; alternatively activated) phenotypes. Macrophages possess P2X7 receptors (Rs) which respond to high concentrations of extracellular ATP under pathological conditions by allowing the non-selective fluxes of cations (Na+, Ca2+, K+). Activation of P2X7Rs by still higher concentrations of ATP, especially after repetitive agonist application, leads to the opening of membrane pores permeable to ~900 Da molecules. For this effect an interaction of the P2X7R with a range of other membrane channels (e.g., P2X4R, transient receptor potential A1 [TRPA1], pannexin-1 hemichannel, ANO6 chloride channel) is required. Macrophage-localized P2X7Rs have to be co-activated with the lipopolysaccharide-sensitive toll-like receptor 4 (TLR4) in order to induce the formation of the inflammasome 3 (NLRP3), which then activates the pro-interleukin-1β (pro-IL-1β)-degrading caspase-1 to lead to IL-1β release. Moreover, inflammatory diseases (e.g., rheumatoid arthritis, Crohn's disease, sepsis, etc.) are generated downstream of the P2X7R-induced upregulation of intracellular second messengers (e.g., phospholipase A2, p38 mitogen-activated kinase, and rho G proteins). In conclusion, P2X7Rs at macrophages appear to be important targets to preserve immune homeostasis with possible therapeutic consequences.
| S-EPMC8745241 | biostudies-literature