scholarly journals Monocyte and macrophage subtypes as paired cell biomarkers for coronary artery disease

2019 ◽  
Vol 104 (9) ◽  
pp. 1343-1352 ◽  
Author(s):  
Kathryn A. Arnold ◽  
John E. Blair ◽  
Jonathan D. Paul ◽  
Atman P. Shah ◽  
Sandeep Nathan ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Artery Disease ◽  
Macrophage Subtypes ◽  
Paired Cell

scholarly journals MONOCYTE AND MACROPHAGE SUBTYPES AS PAIRED CELL BIOMARKERS FOR CORONARY ARTERY DISEASE

2018 ◽  
Vol 71 (11) ◽  
pp. A158
Author(s):  
Kathryn Arnold ◽  
John Blair ◽  
Jonathan Paul ◽  
Atman Shah ◽  
Sandeep Nathan ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Artery Disease ◽  
Macrophage Subtypes ◽  
Paired Cell

scholarly journals Monocyte and Macrophage Subtypes as Paired Cell Biomarkers for Coronary Artery Disease

2018 ◽  
Author(s):  
Kathryn A. Arnold ◽  
John E. Blair ◽  
Jonathan D. Paul ◽  
Atman P. Shah ◽  
Sandeep Nathan ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Mononuclear Cells ◽  
Multivessel Disease ◽  
M2 Macrophages ◽  
Human Coronary Artery ◽  
Single Vessel ◽  
Monocytes And Macrophages ◽  
Artery Disease ◽  
Macrophage Subtypes

ABSTRACTBackground: Monocytes and macrophages are central to atherosclerosis, but how they mark progression of human coronary artery disease (CAD) is unclear. We tested whether patients’ monocyte subtypes paired with their derived macrophage profiles correlate with extent of CAD.Methods: Peripheral blood was collected from 30 patients undergoing cardiac catheterization, and patients were categorized as having no significant CAD, single vessel disease, or multivessel disease according to the number of affected coronary arteries. Mononuclear cells were measured for monocyte markers CD14 and CD16 by flow cytometry, and separate monocytes were cultured into macrophages over 7 days and measured for polarization markers CD86 and CD206.Results: At baseline, patients with greater CAD burden were older with higher rates of statin use, whereas all other characteristics were similar across the spectrum of coronary disease. Non-classical (CD14loCD16hi) and all CD16+ monocytes were elevated in patients with single vessel and multivessel disease compared to those without significant CAD (8.6% and 10.5% vs. 2.8%, p < 0.05), whereas regulatory M2 macrophages (CD206+) were decreased in patients with single vessel and multivessel disease (0.34% and 0.34% vs. 1.4%, p < 0.05). An inverse relationship between paired CD16+ monocytes and M2 macrophages marked CAD severity. CAD was also found to be more tightly associated with CD16+ cells than age or traditional cardiovascular risk factors on multiple regression analysis of these patients.Conclusions: CAD extent is correlated directly with CD16+ monocytes and inversely with M2 (CD206+) macrophages, suggesting circulating monocytes may influence downstream polarization of lesional macrophages. These measures of monocyte and macrophage subtypes hold potential as biomarkers in CAD.

Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chronic Inflammation ◽  
Ex Vivo ◽  
Human Subjects ◽  
Critical Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Tnf Α ◽  
Artery Disease

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.

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