Abstract
In the last decade there have been multiple studies concerning the contribution of endothelial progenitor cells (EPCs) to new vessel formation in different physiological and pathological settings. The process by which EPCs contribute to new vessel formation in adults is termed postnatal vasculogenesis and occurs via four inter-related steps. They must respond to chemoattractant signals and mobilize from the bone marrow to the peripheral blood; home in on sites of new vessel formation; invade and migrate at the same sites; and differentiate into mature endothelial cells (ECs) and/or regulate pre-existing ECs via paracrine or juxtacrine signals. During these four steps, EPCs interact with different physiological compartments, namely bone marrow, peripheral blood, blood vessels and homing tissues. The success of each step depends on the ability of EPCs to interact, adapt and respond to multiple molecular cues. The present review summarizes the interactions between integrins expressed by EPCs and their ligands: extracellular matrix components and cell surface proteins present at sites of postnatal vasculogenesis. The data summarized here indicate that integrins represent a major molecular determinant of EPC function, with different integrin subunits regulating different steps of EPC biology. Specifically, integrin α4β1 is a key regulator of EPC retention and/or mobilization from the bone marrow, while integrins α5β1, α6β1, αvβ3 and αvβ5 are major determinants of EPC homing, invasion, differentiation and paracrine factor production. β2 integrins are the major regulators of EPC transendothelial migration. The relevance of integrins in EPC biology is also demonstrated by many studies that use extracellular matrix-based scaffolds as a clinical tool to improve the vasculogenic functions of EPCs. We propose that targeted and tissue-specific manipulation of EPC integrin-mediated interactions may be crucial to further improve the usage of this cell population as a relevant clinical agent.
Highlights
In the last decade there have been multiple studies concerning the contribution of endothelial progenitor cells (EPCs) to new vessel formation in different physiological and pathological settings
Using an in vivo animal model of hind limb ischemia, these authors showed that CD34+ and vascular endothelial growth factor receptor (VEGFR)-2+ cells were incorporated into newly formed vessels and acquired the expression of endothelial cell (EC) antigens
Circulating BM-derived EPCs were defined as a subset of CD34+ hematopoietic stem cells with the ability to differentiate into the endothelial lineage and express endothelial marker such as von Willebrand Factor and incorporate acetylated Low Density Lipoprotein (Ac-LDL)
Summary
Of bone marrow-derived with chronic ischemic heart disease markers; progenitor cells reduced mortality. Peripheral blood EPCs and on left ventricular function, infarct fraction, no reactive hypertrophy; bone marrow-derived size and reactive hypertrophy progenitor cells. Blindt and colleagues investigated this concept by incorporating integrin-binding cyclic RGD (cRGD) peptide with avb3-integrin-binding capacities into a newly designed polymer stent-coating This stent was analyzed in in vitro and in vivo porcine models for its potential to recruit and bind EPCs and limit coronary neointimal formation. EPCs grown on RGD-g-poly-L-lactic acid scaffolds show increased proliferation, endothelial differentiation and consequent incorporation on wound vessels [125]. Together, these different approaches suggest targeted manipulation of ECM and/or integrin (adhesion) at vascular repair and formation sites may improve EPC function and thereby improve the neovascularization processes
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