ArticleCellular & molecular immunology2013
Notch signaling regulates expression of Mcl-1 and apoptosis in PPD-treated macrophages.
Article in Cellular & molecular immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Dual transcriptomic analysis unraveling the immune landscape and host-pathogen interactions duringiScience · 2025Article
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- Deletion ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
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- Notch signaling pathway involved inFrontiers in cellular and infection microbiology · 2023Article
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- Targets and regulation of microRNA-652-3p in homoeostasis and disease.Journal of molecular medicine (Berlin, Germany) · 2021Review
- Ehrlichia TRP effectors: moonlighting, mimicry and infection.Pathogens and disease · 2021Review
- Notch signaling pathway in infectious diseases: role in the regulation of immune response.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Review
- Review
- Notch Signaling Pathway Is Activated by Sulfate Reducing Bacteria.Frontiers in cellular and infection microbiology · 2021Article
- Regulatory role and mechanism of the inhibition of the Mcl-1 pathway during apoptosis and polarization of H37Rv-infected macrophages.Medicine · 2020Article
- NOTCH1 and DLL4 are involved in the human tuberculosis progression and immune response activation.Tuberculosis (Edinburgh, Scotland) · 2020Article
- Notch-1 Signaling Modulates Macrophage Polarization and Immune Defense againstMicroorganisms · 2020Article
- Review
- NOTCH1 regulates the viability of cholangiocarcinoma cells via 14-3-3 theta.Journal of cell communication and signaling · 2019Article
- Article
- Hall of Fame among Pro-inflammatory Cytokines: Interleukin-6 Gene and Its Transcriptional Regulation Mechanisms.Frontiers in immunology · 2016Review
- Adjunct Strategies for Tuberculosis Vaccines: Modulating Key Immune Cell Regulatory Mechanisms to Potentiate Vaccination.Frontiers in immunology · 2016Review
- Low Dose BCG Infection as a Model for Macrophage Activation Maintaining Cell Viability.Journal of immunology research · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Macrophages are cellular targets for infection by bacteria and viruses. The fate of infected macrophages plays a key role in determining the outcome of the host immune response. Apoptotic cell death of macrophages is considered to be a protective host defense that eliminates pathogens and infected cells. In this study, we investigated the involvement of Notch signaling in regulating apoptosis in macrophages treated with tuberculin purified protein derivative (PPD). Murine bone marrow-derived macrophages (BMMs) treated with PPD or infected with Mycobacterium bovis Bacillus Calmette-Guérin (BCG) induced upregulation of Notch1. This upregulation correlated well with the upregulation of the anti-apoptotic gene mcl-1 both at the transcriptional and translational levels. Decreased levels of Notch1 and Mcl-1 were observed in BMM treated with PPD when a gamma secretase inhibitor (GSI), which inhibits the processing of Notch receptors, was used. Moreover, silencing Notch1 in the macrophage-like cell line RAW264.7 decreased Mcl-1 protein expression, suggesting that Notch1 is critical for Mcl-1 expression in macrophages. A significant increase in apoptotic cells was observed upon treatment of BMM with PPD in the presence of GSI compared to the vehicle-control treated cells. Finally, analysis of the mcl-1 promoter in humans and mice revealed a conserved potential CSL/RBP-Jκ binding site. The association of Notch1 with the mcl-1 promoter was confirmed by chromatin immunoprecipitation. Taken together, these results indicate that Notch1 inhibits apoptosis of macrophages stimulated with PPD by directly controlling the mcl-1 promoter.
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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.