Monocyte subpopulation profiling indicates CDK6-derived cell differentiation and identifies subpopulation-specific miRNA expression sets in acute and stable coronary artery disease View Full Text


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Article Info

DATE

2022-04-04

AUTHORS

Anika Witten, Leonie Martens, Ann-Christin Schäfer, Christian Troidl, Sabine Pankuweit, Ann-Kathrin Vlacil, Raghav Oberoi, Bernhard Schieffer, Karsten Grote, Monika Stoll, Birgit Markus

ABSTRACT

Coronary artery disease (CAD) is a long-lasting inflammatory disease characterized by monocyte migration into the vessel wall leading to clinical events like myocardial infarction (MI). However, the role of monocyte subsets, especially their miRNA-driven differentiation in this scenario is still in its infancy. Here, we characterized monocyte subsets in controls and disease phenotypes of CAD and MI patients using flow cytometry and miRNA and mRNA expression profiling using RNA sequencing. We observed major differences in the miRNA profiles between the classical (CD14++CD16−) and nonclassical (CD14+CD16++) monocyte subsets irrespective of the disease phenotype suggesting the Cyclin-dependent Kinase 6 (CDK6) to be an important player in monocyte maturation. Between control and MI patients, we found a set of miRNAs to be differentially expressed in the nonclassical monocytes and targeting CCND2 (Cyclin D2) that is able to enhance myocardial repair. Interestingly, miRNAs as miR-125b playing a role in vascular calcification were differentially expressed in the classical subset in patients suffering from CAD and not MI in comparison to control samples. In conclusion, our study describes specific peculiarities of monocyte subset miRNA expression in control and diseased samples and provides basis to further functional analysis and to identify new cardiovascular disease treatment targets. More... »

PAGES

5589

References to SciGraph publications

  • 2015-01-25. The mystery of BCL2 family: Bcl-2 proteins and apoptosis: an update in ARCHIVES OF TOXICOLOGY
  • 2013-11-12. MicroRNAs in myocardial ischemia: identifying new targets and tools for treating heart disease. New frontiers for miR-medicine in CELLULAR AND MOLECULAR LIFE SCIENCES
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  • 2013-04-25. TopHat2: accurate alignment of transcriptomes in the presence of insertions, deletions and gene fusions in GENOME BIOLOGY
  • 2018-02-15. The pro-inflammatory phenotype of the human non-classical monocyte subset is attributed to senescence in CELL DEATH & DISEASE
  • 2018-07-31. Immune cell subset differentiation and tissue inflammation in JOURNAL OF HEMATOLOGY & ONCOLOGY
  • 2014-12-05. Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2 in GENOME BIOLOGY
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  • 2017-08-24. Biomechanical Stretch Induces Inflammation, Proliferation, and Migration by Activating NFAT5 in Arterial Smooth Muscle Cells in INFLAMMATION
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/s41598-022-08600-7

    DOI

    http://dx.doi.org/10.1038/s41598-022-08600-7

    DIMENSIONS

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    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/35379829


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    26 schema:description Coronary artery disease (CAD) is a long-lasting inflammatory disease characterized by monocyte migration into the vessel wall leading to clinical events like myocardial infarction (MI). However, the role of monocyte subsets, especially their miRNA-driven differentiation in this scenario is still in its infancy. Here, we characterized monocyte subsets in controls and disease phenotypes of CAD and MI patients using flow cytometry and miRNA and mRNA expression profiling using RNA sequencing. We observed major differences in the miRNA profiles between the classical (CD14++CD16−) and nonclassical (CD14+CD16++) monocyte subsets irrespective of the disease phenotype suggesting the Cyclin-dependent Kinase 6 (CDK6) to be an important player in monocyte maturation. Between control and MI patients, we found a set of miRNAs to be differentially expressed in the nonclassical monocytes and targeting CCND2 (Cyclin D2) that is able to enhance myocardial repair. Interestingly, miRNAs as miR-125b playing a role in vascular calcification were differentially expressed in the classical subset in patients suffering from CAD and not MI in comparison to control samples. In conclusion, our study describes specific peculiarities of monocyte subset miRNA expression in control and diseased samples and provides basis to further functional analysis and to identify new cardiovascular disease treatment targets.
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    62 infarction
    63 inflammatory diseases
    64 kinase 6
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    66 major differences
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    70 miRNA profiles
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    73 monocyte maturation
    74 monocyte migration
    75 monocyte subsets
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    79 nonclassical monocyte subsets
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    81 patients
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