MiRNA-210: A Current Overview

Bavelloni, Alberto; Ramazzotti, Giulia; Poli, Alessandro; Piazzi, Manuela; Focaccia, Enrico; Blalock, William L.; Faenza, Irene

doi:10.21873/anticanres.12107

Cited by 118 publications

(96 citation statements)

References 101 publications

(118 reference statements)

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“…As such, the 8-fold increase in miR-210 may have functional relevance during MC sensitization and subsequent activation, as the increase in miR-210 was sustained during activation. It is known that miR-210 is upregulated during hypoxia, stimulates angiogenesis, induces proliferation, and decreases apoptosis [9]. In an allergic context, miR-210 expression has been shown to increase in mouse lymph nodes and T regulatory cells following dermal chemical sensitization [10], and miR-210 is upregulated in exosomes released by the HMC-1 cell line [11].…”

Section: Resultsmentioning

confidence: 99%

Human Mast Cell Sensitization with IgE Increases miRNA-210 Expression

Just¹,

Ipsen²,

Kruhøffer³

et al. 2019

Int Arch Allergy Immunol

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Background: MicroRNAs (miRNAs) represent important post-transcriptional regulators with a dynamic expression profile during health and disease. Objectives: We explored the miRNA profile of human mast cells (MCs) during sensitization with IgE, during activation through IgE, and relat ed it to prostaglandin D₂ synthesis and histamine release. Method: We investigated the expression pattern of 762 miRNAs during the IgE-mediated sensitization and activation of MCs cultured from CD133+ stem cells that were isolated from allergic asthmatic patients and nonatopic controls. Results: IgE-mediated sensitization increased the expression of miRNA-210 eight-fold. This increase was sustained during IgE-mediated MC activation. Furthermore, we confirmed the increase of the miRNA-132/212 cluster after MC activation. Predicted target genes of miRNA-210/132/212 were enriched in several pathways known to be involved in MC activation. Histamine release was significantly higher in MCs from allergic patients when compared to controls, and a number of miRNAs correlated with histamine release and prostaglandin D₂ synthesis during MC activation. Conclusion: The miRNAs and analysis presented here can help to elucidate the role of miRNAs in mediator release during MC activation. We speculate that miRNA-210 could be important in MC sensitization that leads to allergic symptoms.

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Section: Resultsmentioning

confidence: 99%

Human Mast Cell Sensitization with IgE Increases miRNA-210 Expression

Just¹,

Ipsen²,

Kruhøffer³

et al. 2019

Int Arch Allergy Immunol

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“…Out of 179 different miRNAs, only two were distinctly different in MuSK+ MG patients; miR-210-3p and miR-324-3p were downregulated in MuSK+ MG plasma compared to healthy controls (68). None of these miRNAs have previously been reported dysregulated in immune diseases; however, miR-210-3p has been found dysregulated in several cancers (69) and miR-324-3p has been mentioned as a potential biomarker in the diagnosis of osteoporosis (70).…”

Section: Muscle-specific Tyrosine Kinase Antibody-seropositive Mgmentioning

confidence: 97%

Circulating miRNAs as Potential Biomarkers in Myasthenia Gravis: Tools for Personalized Medicine

Sabre

Punga

2020

Front. Immunol.

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Myasthenia gravis (MG) is an autoimmune disease caused by antibodies which attack receptors at the neuromuscular junction. One of the main difficulties in predicting the clinical course of MG is the heterogeneity of the disease, where disease progression differs greatly depending on the subgroup that the patient is classified into. MG subgroups are classified according to: age of onset [early-onset MG (EOMG; onset ≤ 50 years) versus late-onset MG (LOMG; onset > 50 years]; the presence of a thymoma (thymoma-associated MG); antibody subtype [acetylcholine receptor antibody seropositive (AChR+) and muscle-specific tyrosine kinase antibody seropositive (MuSK+)]; as well as clinical subtypes (ocular versus generalized MG). The diagnostic tests for MG, such as antibody titers, neurophysiological tests, and objective clinical fatigue score, do not necessarily reflect disease progression. Hence, there is a great need for reliable objective biomarkers in MG to follow the disease course as well as the individualized response to therapy toward personalized medicine. In this regard, circulating microRNAs (miRNAs) have emerged as promising potential biomarkers due to their accessibility in body fluids and unique profiles in different diseases, including autoimmune disorders. Several studies on circulating miRNAs in MG subtypes have revealed specific miRNA profiles in patients' sera. In generalized AChR+ EOMG, miR-150-5p and miR-21-5p are the most elevated miRNAs, with lower levels observed upon treatment with immunosuppression and thymectomy. In AChR+ generalized LOMG, the miR-150-5p, miR-21-5p, and miR-30e-5p levels are elevated and decrease in accordance with the clinical response after immunosuppression. In ocular MG, higher levels of miR-30e-5p discriminate patients who will later generalize from those remaining ocular. In contrast, in MuSK+ MG, the levels of the let-7 miRNA family members are elevated. Studies of circulating miRNA profiles in Lrp4 or agrin antibody-seropositive MG are still lacking. This review summarizes the present knowledge of circulating miRNAs in different subgroups of MG.

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“…In human cervical cancer cells, SMAD4 has been identified as a direct target of miR-210 [220]. Hypoxia-inducible factor-1α (HIF-1α) can induce miR-210 expression in various human cell lines [221]. Notably, in synovial fibroblasts from OA patients rCCN2 induces VEGF secretion by raising miR-210 expression which involves phosphatidylinositol 3-kinase (PI3K)-AKT, ERK, and NF-κB/ELK1 signaling [222].…”

Section: Mirna Regulation Of Fibroblast Growth Factor 2 Transformmentioning

confidence: 99%

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

Boehme,

Rolauffs

2018

IJMS

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Osteoarthritis (OA) is a degenerative whole joint disease, for which no preventative or therapeutic biological interventions are available. This is likely due to the fact that OA pathogenesis includes several signaling pathways, whose interactions remain unclear, especially at disease onset. Early OA is characterized by three key events: a rarely considered early phase of proliferation of cartilage-resident cells, in contrast to well-established increased synthesis, and degradation of extracellular matrix components and inflammation, associated with OA progression. We focused on the question, which of these key events are regulated by growth factors, inflammatory cytokines, and/or miRNA abundance. Collectively, we elucidated a specific sequence of the OA key events that are described best as a very early phase of proliferation of human articular cartilage (AC) cells and concomitant anabolic/catabolic effects that are accompanied by incipient pro-inflammatory effects. Many of the reviewed factors appeared able to induce one or two key events. Only one factor, fibroblast growth factor 2 (FGF2), is capable of concomitantly inducing all key events. Moreover, AC cell proliferation cannot be induced and, in fact, is suppressed by inflammatory signaling, suggesting that inflammatory signaling cannot be the sole inductor of all early OA key events, especially at disease onset.

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MiRNA-210: A Current Overview

Cited by 118 publications

References 101 publications

Human Mast Cell Sensitization with IgE Increases miRNA-210 Expression

Human Mast Cell Sensitization with IgE Increases miRNA-210 Expression

Circulating miRNAs as Potential Biomarkers in Myasthenia Gravis: Tools for Personalized Medicine

Onset and Progression of Human Osteoarthritis—Can Growth Factors, Inflammatory Cytokines, or Differential miRNA Expression Concomitantly Induce Proliferation, ECM Degradation, and Inflammation in Articular Cartilage?

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