Extracellular vesicles mediate intercellular communication: Transfer of functionally active microRNAs by microvesicles into phagocytes

Claßen, Laura; Tykocinski, Lars-Oliver; Wiedmann, Felix; Birr, Carolin; Schiller, Petra; Tucher, Christine; Krienke, Stefan; Raab, Marc-Steffen; Blank, Norbert; Lorenz, Hanns Martin; Schiller, Martin

doi:10.1002/eji.201646595

Cited by 36 publications

(32 citation statements)

References 50 publications

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“…21,22 In terms of SLE, miR-34a was reported to be one of the most frequently epigenetically dysregulated miRNAs. 12,23 Our data demonstrated that THRIL silence could not alleviate LPSinduced cell damage when miR-34a was knocked down. Together with the findings that THRIL could repress the expression of miR-34a, here, we briefly concluded that THRIL aggravated HK-2 cell injury induced by LPS might occur via downregulation of miR-34a.…”

Section: Discussionmentioning

confidence: 78%

Retracted: Long noncoding RNA THRIL contributes in lipopolysaccharide‐induced HK‐2 cells injury by sponging miR‐34a

Deng

Luan

Zhang

et al. 2018

J of Cellular Biochemistry

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Systemic lupus erythematosus (SLE) is a chronic autoimmune disease with unknown etiology. Nowadays, several long noncoding RNAs (lncRNAs) have been reported as molecular alterations involved in SLE. This study aimed to reveal the function of TNF‐related and HNRNPL‐related immunoregulatory lncRNA (THRIL) in SLE. Human epithelial HK‐2 cells were exposed to lipopolysaccharide (LPS) to mimic an in vitro SLE model. Then, the functions of THRIL, miR‐34a, and monocyte chemoattractant protein‐1 (MCP‐1), as well as their correlations were detected. LncRNA THRIL was highly expressed in the LPS‐stimulated cells, and THRIL overexpression aggravated LPS‐induced cell damage as cell viability was decreased, and apoptosis and the release of proinflammatory cytokines were increased. THRIL worked as a sponge of microRNA‐34a (miR‐34a) and it could directly target MCP‐1. Furthermore, MCP‐1–activated JNK and Wnt/β‐catenin signaling pathways. In conclusion, this study suggested that lncRNA THRIL might be a key regulator participating in LPS‐induced injury in HK‐2 cells. THRIL overexpression aggravated LPS‐induced injury possibly via sponging miR‐34a, and thus preventing MCP‐1 from degradation by miR‐34a. The THRIL/miR‐34a/MCP‐1 axis might play critical roles in SLE.

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Section: Discussionmentioning

confidence: 78%

Retracted: Long noncoding RNA THRIL contributes in lipopolysaccharide‐induced HK‐2 cells injury by sponging miR‐34a

Deng

Luan

Zhang

et al. 2018

J of Cellular Biochemistry

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“…[21][22][23] During the past few years, circulating miRNAs have drawn much attention in autoimmune diseases including rheumatic diseases. [24][25][26] Exosomes are a kind of extracellular vesicles, which can be found in blood, saliva, urine, cerebrospinal fluid, and milk. Exosomes-encapsulated miRNAs have been shown to modulate immune responses and participate in the pathogenesis of autoimmune diseases.…”

Section: Discussionmentioning

confidence: 99%

MiR‐548a‐3p regulates inflammatory response via TLR4/NF‐κB signaling pathway in rheumatoid arthritis

Wang

Zheng

Gao

et al. 2018

J of Cellular Biochemistry

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Currently published studies have implicated that microRNAs (miRNAs) including exosomes-encapsulated miRNAs play a critical role in rheumatoid arthritis (RA). Previously, we have found that exosomes-encapsulated miR-548a-3p was significantly decreased in serum samples from RA patients by miRNAs microarray analysis. However, little is known of the role of miR-548a-3p in the development and progression of RA. In this study, we aim to investigate the underlying molecular mechanisms of miR-548a-3p in RA, which will provide new insight into understanding the pathogenesis of RA and identifying novel therapeutics targets for this disease. As validated by quantitative real-time polymerase chain reaction (qRT-PCR), the expression of miR-548a-3p in serum exosomes and peripheral blood mononuclear cells (PBMCs) of RA patients (n = 76) was obviously down-regulated compared with healthy controls (n = 20). Serum exosomal miR-548a-3p was negatively associated with levels of CRP, RF, and ESR in serum of patients with RA. MiR-548a-3p could inhibit the proliferation and activation of pTHP-1 cells by regulating the TLR4/NF-κB signaling pathway. Accordingly, exosomes-delivered miR-548a-3p may be a critical factor predicting the disease activity of RA. MiR-548a-3p/TLR4/NF-κB axis can serve as promising targets for RA diagnosis and treatment.

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“…MPs also contain messenger RNA (mRNA) as well as microRNA molecules with regulatory properties. As both mRNA and microRNA can influence the pattern of gene expression of a cell which takes up a particle, MPs could potentially serve as vectors for information transfer between cells …”

Section: Content Of Nuclear Molecules In Microparticlesmentioning

confidence: 99%

“…As both mRNA and microRNA can influence the pattern of gene expression of a cell which takes up a particle, MPs could potentially serve as vectors for information transfer between cells. 34,35 Among products released from dead cells, HMGB1 (high mobility group box 1) is a nonhistone nuclear protein that serves as a prototypic alarmin. 36 HMGB1 is 215 amino acids long and can display immunological activity once released from either dead and dying cells or cells stimulated by LPS or other TLR agonists.…”

Section: Molecules In Microparticlesmentioning

confidence: 99%

Microparticles as autoantigens in systemic lupus erythematosus

Mobarrez

Svenungsson

Pisetsky

2018

Eur J Clin Investigation

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Systemic lupus erythematosus (SLE) is a prototypic autoimmune disease characterized by the production of antibodies to components of the cell nucleus (antinuclear antibodies or ANAs) and the formation of immune complexes with nuclear antigens. These complexes can drive pathogenesis by depositing in the tissue to incite inflammation or induce cytokine production by cells of the innate immune system. While ANAs can bind to purified nuclear molecules, nuclear autoantigens in vivo most likely exist attached to other molecules or embedded in larger structures. Among these structures, microparticles (MPs) are membrane bound vesicles that are released from dead and dying cells by a blebbing process; MPs can also be released during activation of platelets. The presence of MPs in the blood or tissue culture media can be assayed by flow cytometry on the basis of light scattering as well as binding of marker antibodies to identify the cell of origin. As shown by biochemical analyses, MPs contain an ensemble of intracellular components including nuclear, cytoplasmic and membrane molecules. Because of the display of these molecules on the particle surface or in an otherwise accessible form, ANAs, including anti-DNA, can bind to particles. Levels of MPs are increased in the blood of patients with SLE, with flow cytometry demonstrating the presence of IgG-containing particles. In addition to forming immune complexes, MPs can directly stimulate immune responses. Together, these findings suggest an important role of particles in the pathogenesis of SLE and their utility as biomarkers.

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Extracellular vesicles mediate intercellular communication: Transfer of functionally active microRNAs by microvesicles into phagocytes

Cited by 36 publications

References 50 publications

Retracted: Long noncoding RNA THRIL contributes in lipopolysaccharide‐induced HK‐2 cells injury by sponging miR‐34a

Retracted: Long noncoding RNA THRIL contributes in lipopolysaccharide‐induced HK‐2 cells injury by sponging miR‐34a

MiR‐548a‐3p regulates inflammatory response via TLR4/NF‐κB signaling pathway in rheumatoid arthritis

Microparticles as autoantigens in systemic lupus erythematosus

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