ArticleMolecular and cellular biology2012
MicroRNA-155 is required for Mycobacterium bovis BCG-mediated apoptosis of macrophages.
Article in Molecular and cellular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
74 citing papers in PubMed, 135 citations in OpenAlex.
- Role of Exosomes During Mycobacterium Tuberculosis Infection: A Double-Edged Sword.Biomedicines · 2026Review
- Association of Salivary Micro Ribonucleic Acid Levels With the Severity of Severe Acute Respiratory Syndrome Coronavirus 2 Infection in Children.Pediatric discovery · 2026Article
- Upregulation of innate and adaptive immune mechanisms facilitating prevention of gastricFrontiers in immunology · 2026Article
- The TRIM-cancer paradox: BCG as a programmable vaccine platform and a mechanistic probe for rational immunotherapy design.Frontiers in immunology · 2026Review
- Dysregulation of the JNK signaling pathway in tuberculosis: mechanisms and therapeutic strategies.Frontiers in cellular and infection microbiology · 2025Review
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- Differential Expression of miR-146 and miR-155 in Active and Latent Tuberculosis Infection.Iranian journal of public health · 2023Article
- Saliva microRNA Profile in Children with and without Severe SARS-CoV-2 Infection.International journal of molecular sciences · 2023Article
- Different modalities of host cell death and their impact onAmerican journal of physiology. Cell physiology · 2022Review
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- MicroRNAs as Regulators of Phagocytosis.Cells · 2022Review
- Pathophysiology of Atherosclerosis.International journal of molecular sciences · 2022Review
- MicroRNA-155 expression with Brucella infection in vitro and in vivo and decreased serum levels of MicroRNA-155 in patients with brucellosis.Scientific reports · 2022Article
- The Role of TLR2 in Infectious Diseases Caused by Mycobacteria: From Cell Biology to Therapeutic Target.Biology · 2022Review
- miRNA-Mediated Priming of Macrophage M1 Differentiation Differs in Gram-Positive and Gram-Negative Settings.Genes · 2022Article
- MicroRNAs as immune regulators and biomarkers in tuberculosis.Frontiers in immunology · 2022Review
- Immune regulation and emerging roles of noncoding RNAs inFrontiers in immunology · 2022Review
- Progressive Host-Directed Strategies to Potentiate BCG Vaccination Against Tuberculosis.Frontiers in immunology · 2022Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Pathogenic mycobacteria, including Mycobacterium tuberculosis and Mycobacterium bovis, cause significant morbidity and mortality worldwide. However, the vaccine strain Mycobacterium bovis BCG, unlike virulent strains, triggers extensive apoptosis of infected macrophages, a step necessary for the elicitation of robust protective immunity. We here demonstrate that M. bovis BCG triggers Toll-like receptor 2 (TLR2)-dependent microRNA-155 (miR-155) expression, which involves signaling cross talk among phosphatidylinositol 3-kinase (PI3K), protein kinase Cδ (PKCδ), and mitogen-activated protein kinases (MAPKs) and recruitment of NF-κB and c-ETS to miR-155 promoter. Genetic and signaling perturbations presented the evidence that miR-155 regulates PKA signaling by directly targeting a negative regulator of PKA, protein kinase inhibitor alpha (PKI-α). Enhanced activation of PKA signaling resulted in the generation of PKA C-α; phosphorylation of MSK1, cyclic AMP response element binding protein (CREB), and histone H3; and recruitment of phospho-CREB to the apoptotic gene promoters. The miR-155-triggered activation of caspase-3, BAK1, and cytochrome c translocation involved signaling integration of MAPKs and epigenetic or posttranslational modification of histones or CREB. Importantly, M. bovis BCG infection-induced apoptosis was severely compromised in macrophages derived from miR-155 knockout mice. Gain-of-function and loss-of-function studies validated the requirement of miR-155 for M. bovis BCG's ability to trigger apoptosis. Overall, M. bovis BCG-driven miR-155 dictates cell fate decisions of infected macrophages, strongly implicating a novel role for miR-155 in orchestrating cellular reprogramming during immune responses to mycobacterial infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.