Inhibition of Autophagy by MiR-30A Induced by &lt;i&gt;Mycobacteria tuberculosis&lt;/i&gt; as a Possible Mechanism of Immune Escape in Human Macrophages

Chen, Zhi; Wang, Tongjian; Liu, Zhen; Zhang, Guangyu; Wang, Jinhe; Feng, Shisheng; Liang, Juhua

doi:10.7883/yoken.jjid.2014.466

Cited by 82 publications

(64 citation statements)

References 11 publications

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“…The physiological importance of the host miRNA-autophagy interconnection is only beginning to be decoded during the course of bacterial infection. 36,39,40 However, it represents a new understanding of the post-transcriptional regulatory control of autophagy by miRNAs. The exact mechanistic details of host microRNAs in regulating the autophagy process during the course of Leishmania infection remains unknown.…”

Section: Discussionmentioning

confidence: 99%

“…34,43 MIR30A also plays a regulatory role in the autophagic response by targeting BECN1 expression in cancer cells and macrophages infected with Mycobacterium tuberculosis. 34,36 Host microRNA profiling of human monocyte-derived dendritic cells and macrophages infected with different species of Leishmania followed by target analyses have yielded enormous information leading to identification of several key miRNAs that target MAP kinases and signaling cascades modulated during the course of Leishmania infection. 30,31 A recent report suggests induction of MIR210 in a HIF1A-dependent manner in human macrophages infected with L. major.…”

Section: Discussionmentioning

confidence: 99%

“…49 The role of miRNAs in controlling intracellular pathogens such as Mycobacterium and Salmonella is well documented and several microRNAs including MIR30A and MIR155 play key roles in regulating autophagy process by targeting several key molecules regulating the process of autophagy during the course of infection in human macrophages. 36,39 As the information accumulates, there is an urgent need to look into the regulatory mechanisms controlling the host cell autophagy during pathogenic challenge. This information further carries the merit to identify potential antipathogenic therapeutics and decipher the basic information related to the infection process.…”

Section: Discussionmentioning

confidence: 99%

“…34,36 Earlier reports also indicate the regulatory role of MIR30A in autophagy modulation, as overexpression of MIR30A resulted into BECN1-mediated repression of autophagy. 34 To obtain experimental evidence to support BECN1 as a target for MIR30A-3p, we further examined the effect of MIR30A-3p in regulating BECN1 and ATG3 levels in macrophages.…”

Section: Mir30a-3p Negatively Regulates Becn1 Expression In Leishmanimentioning

confidence: 94%

“…17,32,33 The regulatory role of MIR30 family members in downregulation of several genes (e.g., BECN1) involved in autophagy process in cancer cells and infection models has been reported earlier. [34][35][36] Figure 2. Induction of the Leishmania-specific MIR30 family of miRNAs.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA expression profiling ofLeishmania donovani-infected host cells uncovers the regulatory role of MIR30A-3p in host autophagy

et al. 2016

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Leishmania is an obligate intracellular parasite that replicates inside phagolysosomes or parasitophorous vacuoles (PV) of the monocyte/macrophage lineage. It reprograms macrophages and produces a metabolic state conducive to successful infection and multiplication. MicroRNAs (miRNAs), a class of small 22 to 24 nucleotide noncoding regulatory RNAs alter the gene expression and consequently proteome output by targeting mRNAs, may play a regulatory role in modulating host cell functions. In the present study, we demonstrate the novel regulatory role of host microRNA, MIR30A-3p in modulation of host cell macroautophagy/autophagy after infection with L. donovani. Our in vitro studies showed that MIR30A-3p expression was significantly enhanced after L. donovani infection in a time-dependent manner. Transient transfection with a MIR30A-3p inhibitor followed by L. donovani infection promoted the autophagic response and decreased the intracellular parasite burden in both THP-1 cells and human monocytederived macrophages (HsMDM). BECN1/Beclin 1, the mammalian ortholog of yeast Vps30/Atg6, is a key autophagy-promoting protein that plays a key role in the regulation of cell death and survival. We report BECN1-dependent modulation of host cell autophagy in response to L. donovani infection. Pretreatment of L. donovani-infected macrophages with the MIR30A-3p mimic decreased and with antagomir increased the expression of BECN1 protein. We demonstrate that BECN1 is a potential target of MIR30A-3p and this miRNA negatively regulates BECN1 expression. Our present study reveals for the first time a novel role of MIR30A-3p in regulating autophagy-mediated L. donovani elimination by targeting BECN1. The present study has significant impact for the treatment of visceral leishmaniasis.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Mir30a-3p Negatively Regulates Becn1 Expression In Leishmanimentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

MicroRNA expression profiling ofLeishmania donovani-infected host cells uncovers the regulatory role of MIR30A-3p in host autophagy

et al. 2016

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MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

et al. 2019

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Autophagy is a highly conserved catabolic process and fundamental biological process in eukaryotic cells. It recycles intracellular components to provide nutrients during starvation and maintains quality control of organelles and proteins. In addition, autophagy is a well‐organized homeostatic cellular process that is responsible for the removal of damaged organelles and intracellular pathogens. Moreover, it also modulates the innate and adaptive immune systems. Micro ribonucleic acids (microRNAs) are a mature class of post‐transcriptional modulators that are widely expressed in tissues and organs. And, it can suppress gene expression by targeting messenger RNAs for translational repression or, at a lesser extent, degradation. Research indicates that microRNAs regulate autophagy through different pathways, playing an essential role in the treatment of various diseases. It is an important regulator of fundamental cellular processes such as proliferation, autophagy, and cell apoptosis. In this review article, we first review the current knowledge of autophagy and the function of microRNAs. Then, we summarize the mechanism of autophagy and the signaling pathways related to autophagy by citing at least the main proteins involved in the different phases of the process. Second, we introduce other members of RNA and report some examples in various pathologies. Finally, we review the current literature regarding microRNA‐based therapies for cancer, atherosclerosis, cardiac disease, tuberculosis, and viral diseases. MicroRNAs can cause autophagy upregulation or downregulation by targeting genes or affecting autophagy‐related signaling pathways. Therefore, the microRNAs have a huge potential in autophagy regulation, and it is the function as diagnostic and prognostic markers.

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MicroRNAs in the interaction between host–bacterial pathogens: A new perspective

Rad

Goudarzi

et al. 2021

Journal Cellular Physiology

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Gene expression regulation plays a critical role in host-pathogen interactions, and RNAs function is essential in this process. miRNAs are small noncoding, endogenous RNA fragments that affect stability and/or translation of mRNAs, act as major posttranscriptional regulators of gene expression. miRNA is involved in regulating many biological or pathological processes through targeting specific mRNAs, including development, differentiation, apoptosis, cell cycle, cytoskeleton organization, and autophagy. Deregulated microRNA expression is associated with many types of diseases, including cancers, immune disturbances, and infection. miRNAs are a vital section of the host immune response to bacterial-made infection. Bacterial pathogens suppress host miRNA expression for their benefit, promoting survival, replication, and persistence. The role played through miRNAs in interaction with host-bacterial pathogen has been extensively studied in the past 10 years, and knowledge about these staggering molecules' function can clarify the complicated and ambiguous interactions of the host-bacterial pathogen. Here, we review how pathogens prevent the host miRNA expression. We briefly discuss emerging themes in this field, including their role as biomarkers in identifying bacterial infections, as part of the gut microbiota, on host miRNA expression.

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Inhibition of Autophagy by MiR-30A Induced by <i>Mycobacteria tuberculosis</i> as a Possible Mechanism of Immune Escape in Human Macrophages

Cited by 82 publications

References 11 publications

MicroRNA expression profiling ofLeishmania donovani-infected host cells uncovers the regulatory role of MIR30A-3p in host autophagy

MicroRNA expression profiling ofLeishmania donovani-infected host cells uncovers the regulatory role of MIR30A-3p in host autophagy

MicroRNAs play an essential role in autophagy regulation in various disease phenotypes

MicroRNAs in the interaction between host–bacterial pathogens: A new perspective

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