ArticleJournal of cellular and molecular medicine2020
miR-18a promotes Mycobacterial survival in macrophages via inhibiting autophagy by down-regulation of ATM.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 35 citations in OpenAlex.
- PstS1-loaded exosomes promote Mycobacterium tuberculosis infection via miR-122-mediated PI3K/AKT/mTOR activation and autophagy suppression.In vitro cellular & developmental biology. Animal · 2026Article
- Role of Exosomes During Mycobacterium Tuberculosis Infection: A Double-Edged Sword.Biomedicines · 2026Review
- The dual role of the microbiome in chronic wound management.Cell communication and signaling : CCS · 2026Review
- Enhancement of host anti-mycobacterial immunity by green tea hot-water extract is mediated through miR-9-5p-enriched lung extracellular vesicles.Frontiers in immunology · 2026Article
- mTOR Signaling in Macrophages: All Depends on the Context.International journal of molecular sciences · 2025Review
- Autophagy in mycobacterial infections: molecular mechanisms, host-pathogen interactions, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2025Review
- Extracellular vesicles and endothelial dysfunction in infectious diseases.Journal of extracellular biology · 2024Review
- The role ofFrontiers in microbiology · 2024Review
- Current landscape of exosomes in tuberculosis development, diagnosis, and treatment applications.Frontiers in immunology · 2024Review
- Role of Extracellular Vesicles in Immunity and Host Defense.Immunological investigations · 2024Review
- Cargoes of exosomes function as potential biomarkers forFrontiers in immunology · 2023Review
- Novel Biomarker Panel of Let-7d-5p and MiR-140-5p Can Distinguish Latent Tuberculosis Infection from Active Tuberculosis Patients.Infection and drug resistance · 2023Article
- Resistance and Susceptibility Immune Factors at Play duringPathogens (Basel, Switzerland) · 2022Review
- The crosstalk between bacteria and host autophagy: host defense or bacteria offense.Journal of microbiology (Seoul, Korea) · 2022Review
- Understanding microRNAs in the Context of Infection to Find New Treatments against Human Bacterial Pathogens.Antibiotics (Basel, Switzerland) · 2022Review
- MicroRNAs as immune regulators and biomarkers in tuberculosis.Frontiers in immunology · 2022Review
- Regulatory roles of extracellular vesicles in immune responses againstWorld journal of clinical cases · 2021Review
- Crosstalk between exosomes and autophagy: A review of molecular mechanisms and therapies.Journal of cellular and molecular medicine · 2021Review
- Composition and Clinical Significance of Exosomes in Tuberculosis: A Systematic Literature Review.Journal of clinical medicine · 2021Review
- Emerging Role of Exosomes in Tuberculosis: From Immunity Regulations to Vaccine and Immunotherapy.Frontiers in immunology · 2021Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), is one of leading causes of global deaths. This study aimed to explore the role of miR-18a in RAW264.7 cells response to Mtb infection. Exosomes derived from Mtb-infected cells were isolated and further validated by size, transmission electron microscopy and Western blot. RT-PCR was utilized to measure miR-18a expression. Cell viability and ultrastructure were examined by CFU counting, CCK-8 and electron microscope, respectively. Potential target genes of miR-18a were predicted with bioinformatics and further confirmed using RT-PCR, Western blot and laser confocal microscope analysis, respectively. LC3, AMPK and mTOR were measured using Western blot. We found that miR-18a was induced both in Mtb-infected RAW264.7 cells and its derived exosomes compared with the controls. In addition, up-regulation of miR-18a promoted intracellular Mtb survival, attenuated cell viability and reduced LC3-II level, while its down-regulation had the opposite effect. miR-18a overexpression suppressed level of ATM, one possible target of miR-18a, while its underexpression enhanced ATM. We also found that inhibition of ATM induced LC3-II decrease in Mtb-infected cells and could reverse the increase of LC3-II caused by inhibition of miR-18a. Moreover, down-regulation of miR-18a increased p-AMPK level while reduction of ATM could reverse the change. Taken together, our results suggest that miR-18a is up-regulated in macrophages response to Mtb infection, and it promotes intracellular Mtb survival through repressing autophagic process by down-regulation of ATM pathway. This provides new thought for TB pathogenesis, diagnosis and treatment.
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