Please note! This essay has been submitted by a student.
Atherosclerosis accounts for nearly one-third of deaths in ages over 35-years (WHO, 2018). Despite the tremendous progress in biomedical sciences, it is still considered one of the great challenges in medicine owing to its complex pathogenesis. Atherosclerosis causes slow coronary narrowing resulting in stable angina, and pain on exertion. Also, the plaque may rupture, producing acute coronary syndromes including unstable angina, myocardial infarction or even sudden death.
Various risk factors, such as obesity, diabetes mellitus, hypertension, cigarette smoking, hypercholesterolemia, genetic alterations, and familial predisposition can affect the progression of atherosclerosis. It is agreed upon that atherosclerosis starts with endothelial dysfunction then increased adherence of monocytes/macrophages and T-lymphocytes. Monocyte/macrophage infiltrate in the sub-endothelial space accompanied by serum lipid permeation, then the migration of medial smooth muscle cells into the intima.
In addition to their role in lipid uptake, macrophages have a central role in the inflammatory response involved in plaque progression. Accumulating evidence suggests that a subset of hematopoietic stem cells, endothelial progenitor cells (EPCs) that circulate in the blood are involved in atherogenesis. These CD34-positive hematopoietic progenitor cells have not previously been described in human atherosclerotic tissues.
The vascular smooth muscle cells (VSMCs) comprise a major contributor to atherosclerotic plaque development and progression. They have been detected at all stages of atherosclerosis. However, recent technologies for genetic engineering and imaging are mainly performed on animal models, with deficient evidence in humans. A better understanding of their role is required.
Zulli et al. (2005) on their experimental study on rabbits reported that CD34 positive cells are present within the atherosclerotic plaques of rabbits fed high dietary cholesterol. They also reported that several of these cells are also alpha SMC-positive, macrophage-positive, and fibroblast-positive. They suggested that macrophages, smooth muscle cells, and fibroblasts in rabbit atherosclerotic tissue might well be of bone marrow origin.
A more recent study by Kruzliak et al. (2016), reported the absence of CD34(+)/ SMC actin(-) spindle-shaped cells from the fibrous cap. They detected that the predominant cell population was the VSMCs CD34(-)/ SMC actin(+). Few CD34(+)/ SMC actin(+) cells were also present. In our present study, we aim to examine the role of CD34 hematopoietic stem cells in human atherosclerotic tissues and to compare their role with that of macrophages and smooth muscle cells.