miR-99a regulates CD4+ T cell differentiation and attenuates experimental autoimmune encephalomyelitis by mTOR-mediated glycolysis

Gu, Yuting; Yu, Hongshuang; Yang, Wanlin; Wang, Bei; Qian, Fengtao; Cheng, Yih–Shyang; He, Shan; Zhao, Xiaonan; Zhu, Linqiao; Zhang, Yanyun; Jin, Min; Lu, Eryi

doi:10.1016/j.omtn.2021.07.010

Cited by 9 publications

(4 citation statements)

References 42 publications

(68 reference statements)

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“…Accumulating research studies have indicated that abnormal miRNA profile is a distinguishing feature of RA, and some miRNAs have been confirmed to involve the development of this disease [ 16 ]. In this study, decreased miR-129-5p was observed in RA-FLSs compared with normal cells.…”

Section: Discussionmentioning

confidence: 99%

MiR-129-5p Inactivates NF-κB Pathway to Block Rheumatoid Arthritis Development via Targeting BRD4

Chen

2022

Journal of Healthcare Engineering

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Object. Rheumatoid arthritis (RA) is an osteoarticular disease which seriously affects the motor abilities of the patients. MicroRNA disorder has been confirmed as a biomarker event in RA development, and several studies have identified that miR-129-5p is related with the progression of multiple bone diseases. The study attempted to investigate the regulation mechanism of miR-129-5p in RA development. Methods. The abundance of miR-129-5p was detected in the samples including normal tissues and RA tissues and cell lines including human fibroblast-like synoviocytes (hFLSs) and human rheumatoid arthritis fibroblast-like synoviocytes (RA-FLSs). The CCK-8 assay, flow cytometry, Transwell, and ELISA were used to observe the effects of miR-129-5p on the phenotype of RA-FLSs. Moreover, the potential targets of miR-129-5p were identified with TargetScan and dual-luciferase reporter gene assay. Besides, the abundances of the proteins were analyzed with western blot. Results. Decreased miR-129-5p was observed in RA tissues and cells. Increased miR-129-5p obviously blocked the proliferation, inflammatory stress, and migration and remarkably promoted cellular apoptosis. Moreover, BRD4 was confirmed as targets of miR-129-5p, and BRD4 upregulation could partly rescue the inhibition of miR-129-5p on aggressive behaviors of RA-FLSs. Besides, the finding of this study also proved that upregulated miR-129-5p could impede the NF-κB pathway via targeting BRD4. Conclusion. This study suggests that miR-129-5p suppresses the activation of NF-κB pathway to block the progression of RA via targeting BRD4.

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Section: Discussionmentioning

confidence: 99%

MiR-129-5p Inactivates NF-κB Pathway to Block Rheumatoid Arthritis Development via Targeting BRD4

Chen

2022

Journal of Healthcare Engineering

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“…Overexpression of miR-99a, that is frequently down-regulated in RA and SLE, mitigated the development of experimental autoimmune encephalomyelitis (EAE) in mice through the inhibition of mammalian target of rapamycin (mTOR)-dependent glycolysis [231]. Targeting glutamine metabolism is a potential treatment approach in SLE to inhibit plasmablast differentiation [232] and in cancer to overcome tumor immune evasion as well [233].…”

Section: Metabolism and Nutritionmentioning

confidence: 99%

Role of microRNAs in Immune Regulation with Translational and Clinical Applications

Gaál

2024

IJMS

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MicroRNAs (miRNAs) are 19–23 nucleotide long, evolutionarily conserved noncoding RNA molecules that regulate gene expression at the post-transcriptional level. In this review, involvement of miRNAs is summarized in the differentiation and function of immune cells, in anti-infective immune responses, immunodeficiencies and autoimmune diseases. Roles of miRNAs in anticancer immunity and in the transplantation of solid organs and hematopoietic stem cells are also discussed. Major focus is put on the translational clinical applications of miRNAs, including the establishment of noninvasive biomarkers for differential diagnosis and prediction of prognosis. Patient selection and response prediction to biological therapy is one of the most promising fields of application. Replacement or inhibition of miRNAs has enormous therapeutic potential, with constantly expanding possibilities. Although important challenges still await solutions, evaluation of miRNA fingerprints may contribute to an increasingly personalized management of immune dysregulation with a remarkable reduction in toxicity and treatment side effects. More detailed knowledge of the molecular effects of physical exercise and nutrition on the immune system may facilitate self-tailored lifestyle recommendations and advances in prevention.

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“…Overexpression of miR-99a, another anti-inflammatory miRNA, alleviated EAE development by promoting Tregs and inhibiting Th1 cell differentiation through suppression of mechanistic target of rapamycin (mTOR)-regulated glycolysis in CD4+ T cells [ 137 ].…”

Section: Self-extracellular Nucleic Acids In Neuroinflammatory Diseasesmentioning

confidence: 99%

Brain alarm by self-extracellular nucleic acids: from neuroinflammation to neurodegeneration

Kunze,

Fischer,

Marti

et al. 2023

J Biomed Sci

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Neurological disorders such as stroke, multiple sclerosis, as well as the neurodegenerative diseases Parkinson's or Alzheimer's disease are accompanied or even powered by danger associated molecular patterns (DAMPs), defined as endogenous molecules released from stressed or damaged tissue. Besides protein-related DAMPs or “alarmins”, numerous nucleic acid DAMPs exist in body fluids, such as cell-free nuclear and mitochondrial DNA as well as different species of extracellular RNA, collectively termed as self-extracellular nucleic acids (SENAs). Among these, microRNA, long non-coding RNAs, circular RNAs and extracellular ribosomal RNA constitute the majority of RNA-based DAMPs. Upon tissue injury, necrosis or apoptosis, such SENAs are released from neuronal, immune and other cells predominantly in association with extracellular vesicles and may be translocated to target cells where they can induce intracellular regulatory pathways in gene transcription and translation. The majority of SENA-induced signaling reactions in the brain appear to be related to neuroinflammatory processes, often causally associated with the onset or progression of the respective disease. In this review, the impact of the diverse types of SENAs on neuroinflammatory and neurodegenerative diseases will be discussed. Based on the accumulating knowledge in this field, several specific antagonistic approaches are presented that could serve as therapeutic interventions to lower the pathological outcome of the indicated brain disorders.

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miR-99a regulates CD4+ T cell differentiation and attenuates experimental autoimmune encephalomyelitis by mTOR-mediated glycolysis

Cited by 9 publications

References 42 publications

MiR-129-5p Inactivates NF-κB Pathway to Block Rheumatoid Arthritis Development via Targeting BRD4

MiR-129-5p Inactivates NF-κB Pathway to Block Rheumatoid Arthritis Development via Targeting BRD4

Role of microRNAs in Immune Regulation with Translational and Clinical Applications

Brain alarm by self-extracellular nucleic acids: from neuroinflammation to neurodegeneration

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