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Query: UMLS:C0021933 (intussusception)
3,822 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Angiogenesis is the growth of new vessels from preexisting vessels by sprouting and intussusception with ischemia being the major stimulus. Circulating endothelial precursor cells have recently been found to participate in this process. The remodeling of preexisting bridging collateral arterioles, i.e., arteriogenesis, should be a much more efficient mechanism to compensate for the gradual or intermittent occlusion of a major epicardial or peripheral artery. Arteriogenesis is associated with an active growth process. It is probably not dependent on ischemia but initiated by local hemodynamic and mechanical effects on the vessel that occur with increasing blood flow. A variety of growth factors that act not only by stimulating endothelial and smooth muscle cell proliferation and migration, as well as substances that increase recruitment and activation of monocytes have been demonstrated to stimulate angiogenesis and arteriogenesis. Several clinical phase I trials suggest the feasibility and short-term safety of treatment with growth factors or their genes. The VIVA trial, the only phase II trial that has been published in this field, employed VEGF165 by intracoronary infusion followed by several intravenous infusions and did not demonstrate any increase of exercise time or angina by VEGF over placebo. The strong sustained placebo effect was surprising. Concerns about the long-term exacerbation of angiogenesis-dependent pathologic processes, like malignant tumors, atherosclerotic plaque formation and proliferative retinopathies, will require careful follow-up. Pro-angiogenic and pro-arteriogenic therapies may need further sophistication before they enter clinical practice.
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PMID:Angiogenesis and arteriogenesis--not yet for prescription. 1079 81

Blood vessel growth after birth is limited to two major processes. Angiogenesis is the growth of new capillaries by sprouting or intussusception. The major stimulus for angiogenesis is ischemia. In contrast, arteriogenesis describes the remodeling and growth of collateral arteries from a preexisting arteriolar network. Arteriogenesis is induced after the occlusion of a major artery which induces hemodynamic and mechanical effects on the collateral vessel wall which occur with increasing blood flow velocity due to the low pressure at the reentrant site of the collateral vessel. A variety of different cytokines that act by stimulating endothelial and smooth muscle cell proliferation and migration or recruitment and activation of monocytes have been identified to stimulate angiogenesis and/or arteriogenesis (i.e., MCP-1, FGF-2, TGF-beta, VEGF, and GM-CSF). Several clinical trials have been published in that field to suggest the feasibility and safety of treatment with such cytokines or their genes. However, the results indicate that further studies are needed before proangiogenic and proarteriogenic therapies are ready for clinical application.
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PMID:Influence of inflammatory cytokines on arteriogenesis. 1285 53

As a tissue that exhibits rapid cyclical growth and shedding throughout the reproductive life of the female, the human endometrium provides a good model for the study of normal physiological angiogenesis. This paper will review current information on the timing of angiogenesis during the menstrual cycle, the mechanisms involved in endometrial capillary formation, and current information on angiogenesis factors and inhibitors. Based on endothelial cell proliferation studies, the timing of angiogenesis during the menstrual cycle remains unclear. The major mechanism by which endometrial capillaries are formed is probably a mixture of elongation and intussusception, with minimal evidence currently available for sprouting. Numerous angiogenesis factors have been identified in endometrium, the most well studied of which is VEGF. However, to date there is no evidence supporting a relationship between the expression of any given angiogenic factor and the occurrence of angiogenesis in the endometrium. Very limited studies have been undertaken to date on endometrial angiogenesis inhibitors, although the precursors to many of the known proteolytic fragments which act as inhibitors exist in the endometrium. In conclusion, neither the timing of vascular growth during the menstrual cycle nor the mechanisms by which endometrial vessels are formed are currently understood, thus placing major limitations on our understanding of how angiogenesis promoters and inhibitors may act in human endometrium.
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PMID:Endometrial angiogenesis. 1451 49

Two distinct mechanisms, vasculogenesis and angiogenesis implement the formation of the vascular network in the embryo. Vasculogenesis gives rise to the heart and the first primitive vascular plexus inside the embryo and in its surrounding membranes, as the yolk sac circulation. Angiogenesis is responsible for the remodeling and expansion of this network. While vasculogenesis refers to in situ differentiation and growth of blood vessels from mesodermal derived hemangioblasts, angiogenesis comprises two different mechanisms: endothelial sprouting and intussusceptive microvascular growth (IMG). The sprouting process is based on endothelial cell migration, proliferation and tube formation. IMG divides existing vessel lumens by formation and insertion of tissue folds and columns of interstitial tissue into the vessel lumen. The latter are termed interstitial or intervascular tissue structures (ITSs) and tissue pillars or posts. Intussusception also includes the establishment of new vessels by in situ loop formation in the wall of large veins. The molecular regulation of these distinct mechanisms is discussed in respect to the most important positive regulators, VEGF and its receptors flk-1 (KDR) and flt-1, the Angiopoietin/tie system and the ephrin-B/EpH-B system. The cellular mechanisms and the molecular regulation of angiogenesis in the pathological state are summarized and the differences of physiological and pathological angiogenesis elaborated.
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PMID:Vasculogenesis and angiogenesis. 1501 50

Embryonic development is associated with extensive vascular growth and remodeling. We used immunohistochemical, light and electron microscopical techniques, as well as vascular casting methods to study the developing chick embryo kidney with special attention to the interplay between sprouting and intussusceptive vascular growth modes. During inauguration at embryonic day 5 (E5), the early mesonephros was characterised by extensive microvascular sprouting. By E7, the vascular growth mode switched to intussusception, which contributed to rapid kidney vasculature growth up to E11, when the first obvious signs of vascular degeneration were evident. The metanephros underwent similar phases of vascular development inaugurating at E8 with numerous capillary sprouts and changing at E13 to intussusceptive growth, which was responsible for vascular amplification and remodeling. A phenomenal finding was that future renal lobules arose as large glomerular tufts, supplied by large vessels, which were split into smaller intralobular feeding and draining vessels with subsequent formation of solitary glomeruli. This glomerular duplication was achieved by intussusception, i.e., by formation of pillars in rows and their successive merging to delineate the vascular entities. Ultimately, the maturation of the vasculature was achieved by intussusceptive pruning and branching remodeling. An interesting finding was that strong VEGF expression was associated with the sprouting phase of angiogenesis while bFGF was upregulated during the phase of intussusceptive microvascular growth. We conclude that microvascular growth and remodeling in avian kidney follows an adroitly crafted pattern, which entails a precise spaciotemporal interplay between sprouting and intussusceptive angiogenic growth modes supported partly by VEGF and bFGF.
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PMID:Microvascular growth, development, and remodeling in the embryonic avian kidney: the interplay between sprouting and intussusceptive angiogenic mechanisms. 1600 81

In the current study, the contribution of the major angiogenic mechanisms, sprouting and intussusception, to vascular development in the avian lung has been demonstrated. Sprouting guides the emerging vessels to form the primordial vascular plexus, which successively surrounds and encloses the parabronchi. Intussusceptive angiogenesis has an upsurge from embryonic day 15 (E15) and contributes to the remarkably rapid expansion of the capillary plexus. Increased blood flow stimulates formation of pillars (the archetype of intussusception) in rows, their subsequent fusion and concomitant delineation of slender, solitary vascular entities from the disorganized meshwork, thus crafting the organ-specific angioarchitecture. Morphometric investigations revealed that sprouting is preponderant in the early period of development with a peak at E15 but is subsequently supplanted by intussusceptive angiogenesis by the time of hatching. Quantitative RT-PCR revealed that moderate levels of basic FGF (bFGF) and VEGF-A were maintained during the sprouting phase while PDGF-B remained minimal. All three factors were elevated during the intussusceptive phase. Immunohistoreactivity for VEGF was mainly in the epithelial cells, whereas bFGF was confined to the stromal compartment. Temporospatial interplay between sprouting and intussusceptive angiogenesis fabricates a unique vascular angioarchitecture that contributes to the establishment of a highly efficient gas exchange system characteristic of the avian lung.
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PMID:Microvascular endowment in the developing chicken embryo lung. 1724 46

The aim of this in vivo study was to gather quantitative information on the three-dimensional morphology of a new vascular network under the influence of angioactive growth factors. For this purpose, the arteriovenous loop model was used in 10 Lewis rats to generate a bioartificial vascular assembly by means of vascular induction. In this model, an isolated organoid is created in the medial thigh of the animal by methods of tissue engineering. A fibrin gel containing vascular endothelial growth factor (VEGF(165)) and basic fibroblastic growth factor (bFGF) was used as a matrix in the effect group (GF+). Fibrin matrices devoid of growth factors were used as controls (GF-). A microvascular replica of the organoid was created by means of corrosion casting and the network was investigated on stereo-paired images obtained by scanning electron microscopy. Vectors of intercapillary and interbranching distances as well as the diameter of the pores in the intussusceptive events diameter and the ratio of sprouting versus intussusceptive angiogenic events were compared in the two groups. The results were highly significant. In the GF+ group there were more profound three-dimensional morphological traits of angiogenesis, whereas advanced neovascularisation in the phase of remodelling was demonstrated by a higher incidence of intussusception, compared to control. These results illustrate the importance of morphological studies with focus on the generation of three-dimensional vascular networks.
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PMID:The impact of VEGF and bFGF on vascular stereomorphology in the context of angiogenic neo-arborisation after vascular induction. 2162 76

Therapeutic angiogenesis is an attractive strategy to treat patients suffering from peripheral or coronary artery disease. VEGF (vascular endothelial growth factor-A) is the fundamental factor controlling vascular growth in both development and postnatal life. The interplay between the VEGF and Notch signalling pathway has been recently found to regulate the morphogenic events leading to the growth of new vessels by sprouting. Angiogenesis can also take place by an alternative process, i.e. intussusception or vascular splitting. However, little is known about its role in therapeutic angiogenesis and its molecular regulation. In the present article, we briefly review how VEGF dose determines the induction of normal or aberrant angiogenesis and the molecular regulation of sprouting angiogenesis by Notch signalling, and compare this process with intussusception.
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PMID:To sprout or to split? VEGF, Notch and vascular morphogenesis. 2210 1

The cellular and molecular mechanisms of tumor angiogenesis and its prospects for anti-angiogenic cancer therapy are major issues in almost all current concepts of both cancer biology and targeted cancer therapy. Currently, (1) sprouting angiogenesis, (2) vascular co-option, (3) vascular intussusception, (4) vasculogenic mimicry, (5) bone marrow-derived vasculogenesis, (6) cancer stem-like cell-derived vasculogenesis and (7) myeloid cell-driven angiogenesis are all considered to contribute to tumor angiogenesis. Many of these processes have been described in developmental angiogenesis; however, the relative contribution and relevance of these in human brain cancer remain unclear. Preclinical tumor models support a role for sprouting angiogenesis, vascular co-option and myeloid cell-derived angiogenesis in glioma vascularization, whereas a role for the other four mechanisms remains controversial and rather enigmatic. The anti-angiogenesis drug Avastin (Bevacizumab), which targets VEGF, has become one of the most popular cancer drugs in the world. Anti-angiogenic therapy may lead to vascular normalization and as such facilitate conventional cytotoxic chemotherapy. However, preclinical and clinical studies suggest that anti-VEGF therapy using bevacizumab may also lead to a pro-migratory phenotype in therapy resistant glioblastomas and thus actively promote tumor invasion and recurrent tumor growth. This review focusses on (1) mechanisms of tumor angiogenesis in human malignant glioma that are of particular relevance for targeted therapy and (2) controversial issues in tumor angiogenesis such as cancer stem-like cell-derived vasculogenesis and bone-marrow-derived vasculogenesis.
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PMID:Tumor angiogenesis and anti-angiogenic therapy in malignant gliomas revisited. 2314 92

Newly formed microcapillary networks arising in adult organisms by angiogenic and inflammatory stimuli contribute to pathologies such as corneal and retinal blindness, tumor growth, and metastasis. Therapeutic inhibition of pathologic angiogenesis has focused on targeting the VEGF pathway, while comparatively little attention has been given to remodeling of the new microcapillaries into a stabilized, functional, and persistent vascular network. Here, we used a novel reversible model of inflammatory angiogenesis in the rat cornea to investigate endogenous factors rapidly invoked to remodel, normalize and regress microcapillaries as part of the natural response to regain corneal avascularity. Rapid reversal of an inflammatory angiogenic stimulus suppressed granulocytic activity, enhanced recruitment of remodelling macrophages, induced capillary intussusception, and enriched pathways and processes involving immune cells, chemokines, morphogenesis, axonal guidance, and cell motility, adhesion, and cytoskeletal functions. Whole transcriptome gene expression analysis revealed suppression of numerous inflammatory and angiogenic factors and enhancement of endogenous inhibitors. Many of the identified genes function independently of VEGF and represent potentially new targets for molecular control of the critical process of microvascular remodeling and regression in the cornea.
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PMID:Factors regulating capillary remodeling in a reversible model of inflammatory corneal angiogenesis. 2756 55


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