ArticleScientific reports2016
The Transcriptional Foundations of Sp110-mediated Macrophage (RAW264.7) Resistance to Mycobacterium tuberculosis H37Ra.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human tuberculosis (TB), caused by Mycobacterium tuberculosis (Mtb), remains a leading global health problem, causing 1.3 million deaths each year. The nuclear body protein, Sp110, has been linked to TB resistance and previous work showed that it enhances macrophage apoptosis upon Mtb infection. Here, we report on the role of Sp110 in transcriptional regulation of macrophage responses to Mtb through integrated transcriptome and mechanistic studies. Transcriptome analysis revealed that Sp110 regulates genes involved in immune responses, apoptosis, defence responses, and inflammatory responses. Detailed investigation revealed that, in addition to apoptosis-related genes, Sp110 regulates cytokines, chemokines and genes that regulate intracellular survival of Mtb. Moreover, Sp110 regulates miRNA expression in macrophages, with immune and apoptosis-related miRNAs such as miR-125a, miR-146a, miR-155, miR-21a and miR-99b under Sp110 regulation. Additionally, our results showed that Sp110 upregulates BCL2 modifying factor (Bmf) by inhibiting miR-125a, and forced expression of Bmf induces macrophage apoptosis. These findings not only reveal the transcriptional basis of Sp110-mediated macrophage resistance to Mtb, but also suggest potential regulatory roles for Sp110 related to inflammatory responses, miRNA profiles, and the intracellular growth of Mtb.
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