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Current research in the field of vascular biology investigating therapy for treating
various vascular diseases (CVD, CAD, PVD) has now explored the potential of progenitor
cells. Vascular progenitor cells are a subset of primitive bone marrow-derived cells that have
the capacity to proliferate, migrate and differentiate into various mature cell types (Iwata
and Sata, 2007; and Szmitko et al., 2003). These cells possess the ability to restore
vascular function and are capable of homing and differentiating into mature endothelial or
smooth muscle like cells, contributing to vascular remodeling and repair. Needless to say,
discovery of vascular progenitor cells (EPC, SMPC, MPC) has revolutionized the use of cells
as medicines. Therapy based on such progenitor cells is studied under a new emerging
branch termed as `Progenitor Biology' (Metharom and Caplice, 2007).
Among the vascular progenitor cells, endothelial progenitors contribute to
restore vascular homeostasis, and smooth muscle progenitors contribute to pathological
changes (Jevon et al., 2008). Notably, concepts of vascular regeneration and repair were
previously considered limited to the differentiated cells within vascular tissue (Caplice and Doyle,
2005). However, the recent discovery of EPCs with high potential for post-natal vasculogenesis
and vascular homeostasis in adults has revolutionized therapeutic neo-vascularization.
The formation of collateral blood vessel is a regulated process involving the
proliferation, migration and remodeling of endothelial cells from pre-existing vessel (angiogenesis) or
from differentiation of endothelial precursor cells (neo-vascularization) (Faulkes and
Peters, 2005). In analogy with vessel development in the embryo, the
de novo formation of new blood vessels from EPCs has been termed as vasculogenesis. The coronary collateral
vessels formation constitutes a compensatory bypass adaptation to ischemia. Migration and
homing of EPCs to ischemic regions lead to de
novo formation of vascular structures (Leri
and Kajstura, 2005). This vascular response increases blood supply to the myocardium,
reducing the area of hypoxic damage and ultimately the infarct size. The recruitment of
collateral vessels within the coronary circulation is favored by multiple episodes of ischemia,
which provides the stimuli necessary for the growth of vascular structures and increased
blood flow. Needless to say this potential of EPCs is being employed to promote therapeutic
neo-vascularization within the ischemic tissues
(Szmitko et al., 2003). |