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Role of circulating karyocytes in the initiation and progression of atherosclerosis
Helena Chon1, Marianne C Verhaar, Hein A Koomans
1Department of Nephrology and Hypertension, University Medical Center Utrecht, Utrecht, The Netherlands.
Insights
Cardiovascular disease risk factors make leukocytes hypersensitive to normal stimuli, altering gene transcription and promoting inflammation. Monitoring leukocyte gene expression may improve atherosclerosis understanding and treatment guidance.
Area of Science:
- Cardiovascular biology
- Cellular and molecular medicine
- Immunology
Background:
- Cardiovascular disease (CVD) prediction remains challenging, with research focusing on vessel wall cells and blood biochemistry.
- Alterations in circulating blood cells, particularly leukocytes, have been under-investigated despite their role in CVD.
- Existing research has not fully elucidated how cardiovascular risk factors impact leukocyte function at the molecular level.
Purpose of the Study:
- To investigate how cardiovascular risk factors induce redox-dependent changes in leukocyte gene transcription.
- To explore the hypothesis that risk factors render leukocytes hypersensitive to physiological stimuli.
- To establish leukocyte gene expression signatures as potential biomarkers for atherosclerosis progression and treatment.
Main Methods:
- Analysis of redox-dependent changes in leukocyte gene transcription induced by risk factors and physiological stimuli.
- Investigating the role of pro-oxidative states and redox-sensitive transcription factors in leukocyte activation.
- Examining gene expression signatures in leukocytes, specifically monocytes, from individuals with cardiovascular risk factors.
Main Results:
- Cardiovascular risk factors, combined with normal stimuli, induce redox-dependent alterations in leukocyte gene transcription.
- These alterations lead to pathophysiological responses including inflammation, adhesion, and migration.
- Leukocytes become hypersensitive to normal physiological stimuli in the presence of risk factors, promoting a pro-oxidative state.
Conclusions:
- Monitoring leukocyte gene expression signatures can enhance understanding of leukocyte and monocyte function in CVD.
- Leukocyte transcriptomes may serve as tools to assess atherosclerotic disease aggressiveness.
- Gene expression profiling of leukocytes could guide therapeutic strategies for patients with atherosclerosis risk factors.
Abstract:
Cardiovascular disease is still hard to predict in an individual. The main focus in cardiovascular research has been on endothelial cells and vascular smooth muscle cells of the vessel wall and their interactions with the blood flow. Alterations in the properties of the blood have received a lot of attention in biochemical terms. Interestingly, alterations in the properties of circulating cells have received less attention. We propose that presence of 1 or more risk factors together with normal physiological stimuli induce redox-dependent changes in leukocyte gene transcription with pathophysiological responses. Thus, risk factors render leukocytes hypersensitive to normal stimuli. Risk factors can be subdivided into physical and chemical factors. Superimposed on physiological regulators of leukocyte function, these risk factors promote a cellular pro-oxidative state. Redox-sensitive transcription factors are activated, leading to responses involving inflammation, adhesion, migration, and additional reactive oxygen species generation. As a consequence, monitoring of individual gene expression signatures of these cells could well increase our understanding of the mechanisms by which leukocytes and, in particular, monocytes function. Furthermore, transcriptomes of these cells could be used to investigate the aggressiveness of the atherosclerotic process or to guide treatment in the patient with risk factors for atherosclerosis.
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