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Published on: September 26, 2018
Monocyte angiotensin converting enzyme expression may be associated with atherosclerosis rather than arteriosclerosis
Christof Ulrich1, Eric Seibert, Gunnar H Heine
1Department of Internal Medicine II, Martin Luther University, Halle-Wittenberg, Germany.
Insights
Angiotensin converting enzyme (ACE) expression on pro-inflammatory Mo2 monocytes is linked to atherosclerosis in hemodialysis patients. This finding suggests ACE-expressing monocytes may promote plaque buildup, contributing to cardiovascular disease.
Area of Science:
- Immunology
- Cardiovascular Medicine
- Nephrology
Background:
- Circulating monocytes, specifically CD14(++)CD16(+) (Mo2) cells, are associated with cardiovascular risks in hemodialysis patients.
- These Mo2 cells express angiotensin converting enzyme (ACE) and are implicated in chronic inflammation and cardiovascular disease in kidney patients.
- Cardiovascular morbidity stems from atherosclerosis and arteriosclerosis, but the role of ACE-expressing monocytes in these conditions was unclear.
Purpose of the Study:
- To investigate the relationship between ACE expression on Mo2 monocytes and the presence of atherosclerosis and arteriosclerosis.
- To determine if ACE-expressing Mo2 cells are associated with plaque formation or arterial stiffening in hemodialysis patients.
Main Methods:
- A prospective study screened 60 chronic hemodialysis patients.
- Atherosclerosis was assessed using carotid artery ultrasound.
- Arteriosclerosis was measured by pulse pressure, and Mo2 cell ACE expression was quantified via flow cytometry.
Main Results:
- ACE expression on Mo2 monocytes was significantly higher in patients with severe carotid atherosclerosis compared to those with minimal or no atherosclerosis.
- Mo2 cell ACE expression correlated with a quantitative atherosclerosis score and independently predicted carotid plaques.
- No significant relationship was found between Mo2 cell ACE expression and pulse pressure, indicating no association with arteriosclerosis.
Conclusions:
- ACE expression on Mo2 monocytes may contribute to cardiovascular disease in end-stage renal disease patients primarily through the enhancement of atherosclerosis.
- These findings suggest that targeting ACE-expressing Mo2 cells could be a strategy to mitigate atherosclerosis in hemodialysis patients.
Background And Objectives:
Circulating monocytes can be divided into functionally distinct subpopulations according to their surface expression of CD14 and CD16. Monocytes with high-level expression of both antigens (CD14(++)CD16(+), Mo2 cells) are associated with cardiovascular morbidity and mortality in hemodialysis patients. These cells express angiotensin converting enzyme (ACE) on their surface. They are involved in the association of chronic inflammation and cardiovascular disease in kidney patients. Cardiovascular morbidity results from atherosclerosis (plaque-forming, vessel occluding disease) and arteriosclerosis (loss of arterial dampening function). It is unknown whether ACE-expressing proinflammatory monocytes are related to atherosclerosis, arteriosclerosis, or both.
Design, Setting, Participants, & Measurements:
During baseline examination for a prospective study on monocyte ACE expression and mortality, 60 chronic hemodialysis patients of an academic outpatient center were screened for atherosclerosis by carotid artery ultrasound, for arteriosclerosis by pulse pressure measurement, and for ACE expression on Mo2 cells by flow cytometry.
Results:
ACE expression on Mo2 monocytes was significantly higher in patients with severe compared with those with little or no carotid atherosclerosis. Mo2 ACE correlated with a score to semiquantify atherosclerosis and remained a significant predictor of carotid plaques in multivariate analysis including the other univariately associated variables of age, hemoglobin A1c, and albumin. Mo2 ACE was not related to pulse pressure.
Conclusions:
ACE expression on Mo2, although being a known predictor of mortality and cardiovascular disease in end-stage renal disease patients, may act via enhancement of atherosclerosis rather than arteriosclerosis.
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