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Myocarditis
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
George Lazaros, Emilia Lazarou, Dimitris Tousoulis
The work-up of patients presenting with suspected myocarditis includes a variety of tools, including electrocardiogram (ECG), biomarkers, imaging (mainly echocardiography and CMR), and invasive procedures, such as coronary angiography to exclude coronary artery disease and EMB. The diagnostic approach should be individualized depending on clinical presentation. Troponins should be trended in all patients, both for diagnostic purposes and to track disease activity.2 Natriuretic peptides can be useful, especially in patients presenting with HF.38 Viral serology to identify the causative agent, either through circulating antibodies or by polymerase chain reaction, is not generally recommended, taking into consideration the lack of correlation between peripheral blood and EMB findings.23 The presence of heart-specific antibodies is useful for distinguishing between autoimmune myocarditis (presence of autoantibodies in the absence of inflammation on EMB) and inflammatory myocarditis (absence of autoantibodies in the presence of inflammation on EMB).39 Recently, there has been a growing interest in the role of microRNAs (miRNAs) in the pathogenesis, treatment, and early recognition of patients prone to short- and long-term complications. Most important, certain miRNAs, such as miR-155, may be selected as therapeutic targets in acute myocarditis, taking into consideration the inflammation-enhancing properties of the latter.40 The diagnostic ability of the rest of the available screening tools is briefly reported below.
Immune Responses Regulated by Exosomal Mechanisms in Cardiovascular Disease
Published in Shyam S. Bansal, Immune Cells, Inflammation, and Cardiovascular Diseases, 2022
Brooke Lee, Ioannis D. Kyriazis, Ruturaj Patil, Syed Baseeruddin Alvi, Amit Kumar Rai, Mahmood Khan, Venkata Naga Srikanth Garikipati
Studies on pancreatic tumor cells revealed that exosomes containing miR-212-3p lead to a reduced expression of MHC-II molecules in DCs through the downregulation of the regulatory factor X–associated protein (RFXAP) transcription factor (Ding, Zhou et al. 2015). Similarly, miR-203 decreased TLR4 (Toll-like receptor 4) expression in immature DCs when treated with exosomes derived from human pancreatic cancer (PANC-1) cells (Zhou, Chen et al. 2014). Additionally, a detailed study from Montecalvo et al. revealed that exosomes contain miRNA not present in the parent DCs, hinting that EV miRNA may be released at different maturation stages that require unique enrichment factors (Montecalvo, Larregina et al. 2012). Of these miRNAs, miR-148a and miR-451 were found in mature DCs and specifically regulated the unspecified reporter gene used (Montecalvo, Larregina et al. 2012). It was uncovered that the maturation stage of parental DCs affects an exosome’s cargo and the exosome acceptor DCs’ function. miR-155 and miR146a are associated with the inflammatory response to endotoxins (Alexander, Hu et al. 2015). These two miRNAs are negatively correlated with respect to their effects on the severity of the inflammatory response affecting gene expression; miR-155 promotes inflammation, while miR-146a reduces inflammation (Alexander, Hu et al. 2015). The level of inflammation induced by endotoxins was examined and showed that miR-155 promoted endotoxin-induced inflammation, while miR-146a inhibited inflammation (Alexander, Hu et al. 2015).
Role of Epigenetics in Immunity and Immune Response to Vaccination
Published in Mesut Karahan, Synthetic Peptide Vaccine Models, 2021
As the best studied group of ncRNAs, numerous functions have been assigned to various miRNAs. One such miRNA is miR-155 which affects differentiation of CD4+ T lymphocytes into Th1 cells, the development of regulatory T cells (Rodriguez et al. 2007). miR-155 also plays a role in the development of B cell memory. miR-155 targets the transcription factor PU.1 and PU.1 upregulation facilitates IgG1 switch. In cells with low miR-155 expression, IgG1 generation is significantly impaired (Vigorito et al. 2007).
Identification of serum micro-RNAs of early knee osteoarthritis in a cohort of Egyptian patients
Published in Alexandria Journal of Medicine, 2023
Anna Abou-Raya, Mohamed Rizk, Eman AbdelGhani, Nermen AbdelMegid
MicroRNAs (miRNAs) are short, non-coding RNAs that are 19 to 25 nucleotides in length that fine-tune the cell response to a changing environment by modulating the cell transcriptome [35–39]. They regulate gene expression post-transcriptionally by pairing with complementary nucleotide sequences in the 3’-untranslated regions of specific mRNA targets, and have an overarching regulatory role in both normal cellular function and in many diseases including OA [40–42]. MiRNAs have been shown to be involved in the pathology of OA. MicroRNA-155 (miR-155) is a multifunctional miRNA in cells of the immune system whose regulation is highly linked to its role as an immune modulator [43–45]. MiR-155-5p can control cell proliferation and apoptosis in many diseases [44]. However, when deregulated, miR-155 contributes to the development of chronic inflammation, autoimmunity, cancer, and fibrosis [43]. MiR-155-5p has been reported to be expressed and identified as a potent regulator of cytokine expression in inflammatory arthritis like rheumatoid arthritis [43–45]. MiR-136-5p has been shown to effectively enhance inflammatory factors and chemokines via activating nuclear factor kappa beta (NF-κB)/A20 signaling in the IL-17-mediated inflammatory response both in vitro and in vivo. Over-expression of miR-136-5p appears to inhibit cartilage degeneration [46,47].
Upregulation of miR-33 and miR-155 by gum acacia mitigates hyperlipidaemia and inflammation but not weight increase induced by Western diet ingestion in mice
Published in Archives of Physiology and Biochemistry, 2023
In particular, miR-33, located at the intron region of sterol regulatory element binding protein 2 (SREBP2) gene, was involved in many aspects of lipid metabolism such as high density lipoprotein (HDL) biogenesis, metabolism of fatty acids, triglycerides and cholesterol in addition to its role in insulin signalling, inflammation and cell proliferation (Corona-Meraz et al. 2019). MiR-33 was recently found to play an important role in atherosclerosis initiation and progression (Koyama et al. 2019). Similarly, MiR-155 is involved in the pathogenesis of several conditions as inflammation, cancer and atherosclerosis (Bruen et al. 2019). It was previously found that upregulation of miR-155 was protective against the development of liver steatosis and promoted liver regeneration after partial hepatectomy (Lin et al. 2018). However, other studies found that miR-155 inhibition by anti-miR-155 exhibited a therapeutic potential and decreased the development of liver steatosis and fibrosis in vitro and in vivo (Eissa and Artlett 2019, Liu et al. 2020).
Shenlian extract attenuates myocardial ischaemia-reperfusion injury via inhibiting M1 macrophage polarization by silencing miR-155
Published in Pharmaceutical Biology, 2022
Min Song, Xihe Cui, Jing Zhang, Yujie Li, Jingjing Li, Yuanlong Zang, Qi Li, Qing Yang, Ying Chen, Weiyan Cai, Xiaogang Weng, Yajie Wang, Xiaoxin Zhu
Next, we examined the expression of miR-155in vitro. In Figure 7(A,B), gene expression of miR-155 increased significantly in LPS-treated macrophages in comparison with control macrophages, and in co-treated LPS and SL macrophages gene, expression of miR-155 reduced in a dose-dependent compared with LPS-treated macrophages (Figure 7(A,B), p < 0.05). Meanwhile, fluorescence in situ hybridization results showed that miR-155/F4/80 positive makers in the model group were more than that in the control group, and in the SL groups miR-155/F4/80 expressions were less than that in the model group (Figure 7(C,D), p < 0.05). Furthermore, fluorescence in situ hybridization of miR-155/CD86 results illustrated that miR-155/CD86 positive signals in the model group raised significantly compared with the control group, but in the SL groups, miR-155/CD86 expressions decreased notably compared with the model group (Figure 7(E,F), p < 0.05).