MicroRNA-155 Promotes Autophagy to Eliminate Intracellular Mycobacteria by Targeting Rheb
Open accessAbstract
Mycobacterium tuberculosis is a hard-to-eradicate intracellular pathogen that infects one-third of the global population. It can live within macrophages owning to its ability to arrest phagolysosome biogenesis. Autophagy has recently been identified as an effective way to control the intracellular mycobacteria by enhancing phagosome maturation. In the present study, we demonstrate a novel role of miR-155 in regulating the autophagy-mediated anti-mycobacterial response. Both in vivo and in vitro studies showed that miR-155 expression was significantly enhanced after mycobacterial infection. Forced expression of miR-155 accelerated the autophagic response in macrophages, thus promoting the maturation of mycobacterial phagosomes and decreasing the survival rate of intracellular mycobacteria, while transfection with miR-155 inhibitor increased mycobacterial survival. However, macrophage-mediated mycobacterial phagocytosis was not affected after miR-155 overexpression or inhibition. Furthermore, blocking autophagy with specific inhibitor 3-methyladenine or silencing of autophagy related gene 7 (Atg7) reduced the ability of miR-155 to promote autophagy and mycobacterial elimination. More importantly, our study demonstrated that miR-155 bound to the 3'-untranslated region of Ras homologue enriched in brain (Rheb), a negative regulator of autophagy, accelerated the process of autophagy and sequential killing of intracellular mycobacteria by suppressing Rheb expression. Our results reveal a novel role of miR-155 in regulating autophagy-mediated mycobacterial elimination by targeting Rheb, and provide potential targets for clinical treatment.
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Mtb induces miR-155, which targets Rheb, boosts autophagy in macrophages, promotes phagosome maturation, and decreases intracellular mycobacteria survival.
“Mtb induces expression of miR-155, which, by targeting Ras homologue enriched in brain (Rheb), boosts the autophagic response in macrophages, thus promoting the maturation of phagosomes and decreasing the survival rate of intracellular mycobacteria”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [162]
Uptake remains unchanged by miR-155 modulation.
“Uptake remains unchanged by miR-155 modulation [162].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [162]
Transfection with miR-155 inhibitor increases mycobacterial survival.
“while transfection with miR-155 inhibitor increases mycobacterial survival.”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [162]
miR-155 exerts its effect on phagosomes and intracellular mycobacteria survival by binding to the 3′-untranslated region of Rheb, a negative regulator of autophagy.
“This effect is exerted upon binding of miR-155 to the 3′-untranslated region of RAS homolog enriched in brain (Rheb), which is a negative regulator of autophagy (79).”
From Macrophage defense mechanisms against intracellular bacteria (2015) · cites this paper as [79]
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- Authors
- Wang, J., Yang, K., Zhou, L., MinhaoWu, Wu, Y., Zhu, M., Lai, X., Chen, T., Feng, L., Li, M., Huang, C., Zhong, Q., & Huang, X.
- Affiliations
- Sun Yat-sen University (CN)
- Center for Tuberculosis Control of Guangdong Province (CN)
- Corresponding author
- Zhong, Qiu
- Huang, Xi
- ORCID
- Venue
- PLoS Pathogens
- Publisher
- Public Library of Science (PLoS)
- Published
- 2013-10-10
- Volume
- 9
- Issue
- 10
- Pages
- e1003697
- ISSN
- 1553-7366 (ISSN-L)
- 1553-7374
- PMC
- PMC3795043
- OpenAlex
- W2037432461
- Cited by
- 265
- References
- 65
- Citations by year
- 2026: 13 · 2025: 16 · 2024: 14 · 2023: 13 · 2022: 19 · 2021: 20 · 2020: 24 · 2019: 15 · 2018: 29 · 2017: 22 · 2016: 29 · 2015: 28 · 2014: 20 · 2013: 2
- FWCI
- 19.21
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS Pathogens (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Wayne State University
- National Natural Science Foundation of China (81261160323, U0832006, 81172811, 2009010058, 31200662, 30972763)
- Natural Science Foundation of Guangdong Province (2011Y035, 10251008901000013, S2012040006680, 2009010058)
- Specialized Research Fund for the Doctoral Program of Higher Education of China (20100171110047)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Keywords
- miR-155, Rheb, autophagy, Mycobacterium tuberculosis, macrophages, phagosome maturation, phagolysosome biogenesis, ATG7, 3' untranslated region, antimycobacterial immunity, microRNA regulation
- MeSH terms
- Autophagy-Related Protein 7, Ras Homolog Enriched in Brain Protein, Animals, Autophagy, Cell Line, Gene Expression Regulation, Macrophages, Mice, Inbred BALB C, Microtubule-Associated Proteins, Mycobacterium tuberculosis, Neuropeptides, Tuberculosis, Monomeric GTP-Binding Proteins, MicroRNAs, Microbial Viability, Mice
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