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These and subsequent observations in nondevelopmental settings have provided a detailed histologi cal account of new blood vessel formation, which can be summarized as follows.Th in, cy top la sm icprocess es are then TABLE. The above list, compiled on the basis of discipline, summarizes some of the other settings that are likely to benefit from therapeutic manipulation of angiogenesis.Migrating endothelial cells elongate and align with one another to form a capil lary sprout, and endothelial cell division, which occurs proximal to the migrating tip, further increases the length of the sprout.The solid sprout gradually develops a lumen proximal to the region of proliferation.Contigu ous tubular sprouts anastomose at their tips to form a functional capillary loop in which blood flow is soon established.Vessel maturation is accomplished by reconstitution of the basement membrane.Together, these cel lular functions contribute to the process of capillary morphogenesis, ie, the Ritodrine hydrochloride formation of patent, endotheliumlined, tubelike structures.The mainte nance of endothelial quiescence is Octocrilene thought to be due to the presence of endogenous negative regulators, since positive regulators are frequently detected in adult tissues in which there is apparently no angiogenesis.The converse is also true, namely, that positive and negative regulators often coexist in tissues in which endothelial cell turnover is increased.This has led to the notion that endothelial activation status is determined by a balance between positive and negative regulators: in activated nate, whereas endothelial quiescence is achieved and maintained by the dominance of negative regulators gression to describe the passage from the prevascular to the vascular phase genic switch is also applicable to developmental and physiological as well as pathological angiogenesis.Although this still remains to be definitively demon strated in vivo, the current working hypothesis is that the switch involves either the induction of a positive regula tor andor the loss of a negative regulator.The multiple cell functions that occur during angio genesis can be classified into a phase of activation and a phase of resolution. While a great deal is known about the factors that induce the activation phase, very little is known about the factors involved in the phase of resolu tion, in which it is assumed that the dominant activity of negative regulators is called into play.A large num ulate angiogenesis in the experimental setting.However, with the exception of VEGFVPF, for almost all of these factors defini tive studies are still required to demonstrate their role in the endogenous regulation of angiogenesis.If the latter hypothesis is correct, it would be necessary to assume that endothelial cells have the inherent capacity to synthesize their own basement membrane and organize into capillarylike tubes and that this is mediated in part by the autocrine activity of endogenous regulators.With respect to acti vated endothelium, an important distinction must be made between physiological and pathological settings: although many of the same positive and negative regula tors are operative in both, endothelial cell proliferation in the former is tightly controlled, whereas in the latter, uncontrolled angiogenesis implies continuous domi nance of positive regulators, which results in unchecked endothelial cell growth.

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