Arterial regeneration by collateral artery growth (arteriogenesis) (original) (raw)
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Arteriogenesis The Development and Growth of Collateral Arteries
Microcirculation, 2003
In patients with atherosclerotic vascular diseases, collateral vessels bypassing major arterial obstructions have frequently been observed. This may explain why some patients remain without symptoms or signs of ischemia. The term "arteriogenesis" was introduced to differentiate the formation of collateral arteries from angiogenesis, which mainly occurs in the ischemic, collateral flowdependent tissue. Many observations in various animal models and humans support that the remodeling of preexisting collateral vessels is the mechanism of collateral artery formation. This remodeling process seems to be mainly flowmediated. It involves endothelial cell activation, basal membrane degradation, leukocyte invasion, proliferation of vascular cells, neointima formation (in most species studied), and changes of the extracellular matrix. The contribution of ischemia to arteriogenesis is still unclear, but arteriogenesis clearly can occur in the absence of any significant ischemia. It is questionable, whether collateral arteries also form de novo in ischemic vascular diseases. A better understanding of the mechanisms of arteriogenesis will be important for the design of more effective strategies for the treatment of patients with ischemic vascular diseases. Microcirculation (2003) 10, 83-97. Arteriogenesis A Helisch and W Schaper 84 Arteriogenesis A Helisch and W Schaper 85 Arteriogenesis A Helisch and W Schaper 91 Arteriogenesis A Helisch and W Schaper 93 Arteriogenesis A Helisch and W Schaper 94
Insights into Pathways of Arteriogenesis
Current Pharmaceutical Biotechnology, 2007
The compensatory growth of blood vessels after major arterial occlusions has been termed arteriogenesis. Although having some characteristics in common with angiogenesis, marked differences between both forms of vascular growth exist relating to triggers, underlying mechanisms and physiologic effects.
Acta Biochimica et Biophysica Sinica, 2008
Patients with occlusive atherosclerotic vascular diseases have frequently developed collateral blood vessels that bypass areas of arterial obstructions. The growth of these collateral arteries has been termed "arteriogenesis", which describes the process of a small arteriole's transformation into a much larger conductance artery. In recent years, intensive investigations using various animal models have been performed to unravel the molecular mechanisms of arteriogenesis. The increasing evidence suggests that arteriogenesis seems to be triggered mainly by fluid shear stress, which is induced by the altered blood flow conditions after an arterial occlusion. Arteriogenesis involves endothelial cell activation, basal membrane degradation, leukocyte invasion, proliferation of vascular cells, neointima formation (in most species studied), changes of the extracellular matrix and cytokine participation. This paper is an in-depth review of the research critical to recent advances in the field of arteriogenesis that have provided a better understanding of its mechanisms.
Factors Regulating Arteriogenesis
Arteriosclerosis, Thrombosis, and Vascular Biology, 2003
Growth of collateral vessels is potentially able to preserve structure and a variable degree of function in subtended tissues in the presence of arterial occlusions. The process of transformation of a small arteriole into much larger conductance artery is called arteriogenesis. Small arterioles that interconnect side branches proximal from the arterial occlusion with distal ones experience increased fluid shear stress because of the increased blood flow velocity attributable to the pressure gradient along the bridging collaterals. This activates the endothelium and leads to monocyte adhesion and infiltration with the subsequent production of growth factors and proteases. Preexistent arterioles are essential. Their presence is genetically determined. Arteriogenesis is not organ-or species-specific; coronary or peripheral collateral vessels develop following the same design principles in mice, rats, rabbits, or dogs. In contrast to angiogenesis, arteriogenesis is not dependent on the presence of hypoxia/ischemia. (Arterioscler Thromb Vasc Biol. 2003;23:1143-1151.)
Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth
Physiology, 1999
After birth, new blood vessel formation proceeds via angiogenesis or arteriogenesis. Angiogenesis (capillary sprouting) results in higher capillary density. Arteriogenesis (rapid proliferation of collateral arteries) is potentially able to significantly alter the outcome of coronary and peripheral artery disease. The processes share some growth features but differ in many aspects.
… , and vascular biology, 2004
Objective-The role of fluid shear stress (FSS) in collateral vessel growth remains disputed and prospective in vivo experiments to test its morphogenic power are rare. Therefore, we studied the influence of FSS on arteriogenesis in a new model with extremely high levels of collateral flow and FSS in pig and rabbit hind limbs. Methods and Results-A side-to-side anastomosis was created between the distal stump of one of the bilaterally occluded femoral arteries with the accompanying vein. This clamps the collateral reentry pressure at venous levels and increases collateral flow, which is directed to a large part into the venous system. This decreases circumferential wall stress and markedly increases FSS. One week after anastomosis, angiographic number and size of collaterals were significantly increased. Maximal collateral flow exceeded by 2.3-fold that obtained in the ligature-only hind limb. Capillary density increased in lower leg muscles. Immunohistochemistry revealed augmented proliferative activity of endothelial and smooth muscle cells. Intercellular adhesion molecule-1 and vascular cell adhesion molecule (VCAM)-1 were upregulated, and monocyte invasion was markedly increased. In 2-dimensional gels, actin-regulating cofilin1 and cofilin2, destrin, and transgelin2 showed the highest degree of differential regulation. Conclusions-High levels of FSS cause a strong arteriogenic response, reinstate cellular proliferation, stimulate cytoskeletal rearrangement, and normalize maximal conductance. FSS is the initiating molding force in arteriogenesis.
Development of collateral vessels: A new paradigm in CAM angiogenesis model
Microvascular Research, 2016
The chorioallantoic membrane (CAM) assay is one of the most widely used models to study angiogenesis. In this study, collateral vessel development is reported in CAM assay useful in analysis of angiogenesis. Four days old white Leghorn fertilized chicken eggs were inoculated with vehicle, standard or test angiogenesis inhibitor using standard protocol. Central vessel growth was seen tapering down and collateral vessels were developed from lower side of chorioallantoic membrane moving upward in 12 days old standard or test treated CAMs. In absence of central vessel, collateral blood supply helped in survival of embryos. Hence, development of collateral vessels was used for ranking of blood vessels and angiogenesis in addition to well-known standard parameters related to central vessel. The finding could differentiate molecules inhibiting angiogenesis with or without collateralization which is crucial in antiangiogenic therapy used for cardiovascular diseases and cancer. This study proposes a new avenue to distinguish pro-angiogenic molecules from anti-angiogenic ones as well as anti-angiogenic molecules which may or may not support alternative vascularization pathway that would have great impact on future angiogenic and anti-angiogenic therapy.