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New Vessel Formation (new + vessel_formation)
Selected AbstractsAngiogenesis of the heartMICROSCOPY RESEARCH AND TECHNIQUE, Issue 2 2003Michael J.B. Kutryk Abstract Despite continued advances in the prevention and treatment of coronary artery disease, there are still a large number of patients who are not candidates for the conventional revascularization techniques of balloon angioplasty and stenting, or coronary artery bypass grafting (CABG). Therapeutic angiogenesis, in the form of the administration of growth factor protein or gene therapy, has emerged as a promising new method of treatment for patients with coronary artery disease. The goal of this strategy is to promote the development of supplemental blood conduits that will act as endogenous bypass vessels. New vessel formation occurs through the processes of angiogenesis, vasculogenesis, and arteriogenesis, under the control of growth factors such as those that belong to the vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF) and angiopoeitin (Ang) families of molecules. Preclinical studies have suggested that such an approach is both feasible and effective; however many questions remain to be answered. This review will address the elements of pharmacologic revascularization, focusing on gene and protein-based therapy. The important growth factors, the vector (for gene therapy), routes of delivery, the desired therapeutic effect, and quantifiable clinical end points for trials of angiogenesis will all be addressed. Microsc. Res. Tech. 60:138,158, 2003. © 2003 Wiley-Liss, Inc. [source] USE OF PORCINE SMALL INTESTINAL SUBMUCOSA IN BLADDER AUGMENTATION IN RABBIT: LONG-TERM HISTOLOGICAL OUTCOMEANZ JOURNAL OF SURGERY, Issue 1-2 2008Ali Ayyildiz Aim: To investigate long-term histological features of bladder augmentation using porcine small intestine submucosa (SIS) in a rabbit model. Materials and method: Sixteen New Zealand rabbits were used. Porcine SIS was provided by a manufactured formation derived from the pig. After partial cystectomy was carried out on the bladder, a single layer of SIS (Cook® -SIS Technology, Cook Biotech Incorporated, West Lafayette, IN, USA) (2 × 5 cm) was sewn to bladder with continuous 5/0 vicryl suture material in a watertight manner. Urinary diversion was not used. The rabbits were killed 12 months later and perivesical fat was removed together with bladder. The 5-,m preparations taken from the samples were stained with haematoxylin,eosin and Mason's trichrome dye. S-100 and F8 stains were also used for immunohistochemical investigations. Results: The macroscopic view of bladder was normal. SIS was indistinguishable from normal bladder wall, but the region of the graft had a slight white coloration. Microscopic observations showed the continuity of transitional epithelium of host bladder tissue on SIS material. Detrusor and serosal layers were formed and these layers were indistinguishable from host bladder. Fibroblasts were scattered among the collagen fibrils. New vessel formations were present without lymphatic proliferation. Nerve regeneration was excellent. No inflammation was observed in normal and regenerated bladder wall. Conclusion: At the end of 12 months, the long-term histological features of bladder augmentation with porcine SIS in a rabbit model, such as presence of new vessel formations, nerve regeneration, collagen and smooth muscle regenerations, which were indistinguishable from original bladder, and the absence of inflammation, showed that SIS seems to be a viable alternative to the use of intestine in bladder augmentation. [source] Potential manipulation of endothelial progenitor cells in diabetes and its complicationsDIABETES OBESITY & METABOLISM, Issue 7 2010G. P. Fadini Diabetes mellitus increases cardiovascular risk through its negative impact on vascular endothelium. Although glucotoxicity and lipotoxicity account for endothelial cell damage, endothelial repair is also affected by diabetes. Endothelial progenitor cells (EPCs) are involved in the maintenance of endothelial homoeostasis and in the process of new vessel formation. For these reasons, EPCs are thought to have a protective impact within the cardiovascular system. In addition, EPCs appear to modulate the functioning of other organs, providing neurotropic signals and promoting repair of the glomerular endothelium. The exact mechanisms by which EPCs provide cardiovascular protection are unknown and the definition of EPCs is not standardized. Notwithstanding these limitations, the literature consistently indicates that EPCs are altered in type 1 and type 2 diabetes and in virtually all diabetic complications. Moreover, experimental models suggest that EPC-based therapies might help prevent or reverse the features of end-organ complications. This identifies EPCs as having a novel pathogenic role in diabetes and being a potential therapeutic target. Several ways of favourably modulating EPCs have been identified, including lifestyle intervention, commonly used medications and cell-based approaches. Herein, we provide a comprehensive overview of EPC pathophysiology and the potential for EPC modulation in diabetes. [source] Angiopoietin/tie-2 as mediators of angiogenesis: a role in congestive heart failure?EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2004A. Y. Chong Abstract Angiogenic factors, in particular vascular endothelial growth factor (VEGF) and the angiopoietins, Ang-1 and -2, have recently generated significant interest, especially in oncology. The process of angiogenesis is also thought to occur in response to ischaemic conditions, which lie at the core of cardiovascular disease states such as coronary artery disease and congestive heart failure. However, current data do not conclusively show evidence of angiogenesis per se in these conditions, despite (for example) the presence of high levels of VEGF and Ang-2. High levels of these angiogenic factors in heart disease also have not translated into clinically significant new vessel formation, as in accelerated cancer growth or proliferative retinopathy. Indeed, we would hypothesize that these angiogenic markers , especially the angiopoietins , do not necessarily translate into new vessel formation in congestive heart failure (CHF), but may well reflect disturbances of endothelial integrity in CHF. [source] Intravital insights in skin wound healing using the mouse dorsal skin fold chamberJOURNAL OF ANATOMY, Issue 6 2007Heiko Sorg Abstract The skin fold chamber is one of the most accepted animal models for studying the microcirculation both in health and disease. Here we describe for the first time the alternative use of the skin fold chamber in mice for intravital microscopic investigation of skin regeneration after creating a full dermal thickness wound. The dorsal skin fold chamber was implanted in hairless SKH1-hr mice and a full dermal thickness wound (area ~4 mm2) was created. By means of intravital fluorescence microscopy, the kinetics of wound healing were analyzed for 12 days post wounding with assessment of epithelialization and nutritive perfusion. The morphology of the regenerating skin was characterized by hematoxylin-eosin histology and immunohistochemistry for proliferation and microvessel density. The model allows the continuous visualization of wound closure with complete epithelialization at day 12. Furthermore, a sola cutis se reficientis could be described by an inner circular ring of vessels at the wound margin surrounded by outer radial passing vessels. Inner circular vessels presented initially with large diameters and matured towards diameters of less than 15 µm for conversion into radial spreading outer vessels. Furthermore, wound healing showed all diverse core issues of skin repair. In summary, we were able to establish a model for the analysis of microcirculation in the healing skin of the mouse. This versatile model allows distinct analysis of new vessel formation and maturation in regenerating skin as well as evaluation of skin healing under different pathologic conditions. [source] Basement membrane thickening and clinical features of children with asthmaALLERGY, Issue 6 2007E. S. Kim Background:, Asthma is a chronic inflammatory disease, characterized by airway inflammation, bronchial hyper-responsiveness, and airway obstruction. Although asthma induces partially reversible airway obstruction, obstruction can sometimes become irreversible. This may be a consequence of airway remodeling, which includes a number of structural changes, such as epithelial detachment, basement membrane (BM) thickening, smooth muscle hypertrophy, and new vessel formation. This study evaluated children with asthma for the presence of BM thickening. Methods:, Eighteen children with asthma and 24 control subjects underwent flexible bronchoscopy with endobronchial biopsy. Light microscopy was used to measure BM thickness in paraffin-embedded biopsy sections. The association between BM thickening and age, sex, duration of asthma, asthma severity, FEV1, FEV1/FVC, FEF25,75%, methacholine PC20, eosinophil count, and presence of atopy was examined. Results:, Basement membrane thickness was greater in subjects with asthma (8.3 ± 1.4 ,M) than in control subjects (6.8 ± 1.3 ,M, P = 0.0008). Multiple regression analysis revealed that sex, FEV1/FVC, total IgE, and atopy (IgE for Dermatophagoides pteronyssinus >0.34 kUA/l) were significant predictive factors for BM thickness. There was no significant association between BM thickness and age, duration of asthma, FEV1, FEF25,75%, methacholine PC20, eosinophil count, or asthma severity. Conclusions:, Basement membrane thickening has been known to be present in children with asthma. In addition, we report an association between BM thickness and sex, FEV1/FVC, total IgE, and the presence of IgE specific to D. pteronyssinus. [source] Differential expression of stromal cell,derived factor 1 and its receptor CXCR4 in the skin and endothelial cells of systemic sclerosis patients: Pathogenetic implicationsARTHRITIS & RHEUMATISM, Issue 9 2006Paola Cipriani Objective Systemic sclerosis (SSc) is characterized by early endothelial damage evolving to vascular desertification. Stromal cell,derived factor 1 (SDF-1) and its receptor CXCR4 regulate specific steps in new vessel formation. We undertook this study to determine whether an alteration of the SDF-1/CXCR4 axis might be involved in the pathogenetic mechanisms following ischemic damage during SSc. Methods We enrolled 36 SSc patients and 15 controls. Skin biopsy samples were obtained from each subject, and the expression of SDF-1 and CXCR4 was assessed by immunohistochemistry, reverse transcription,polymerase chain reaction (RT-PCR), and Western blot analyses. Furthermore, isolated microvascular endothelial cells (MVECs) from 4 patients with diffuse cutaneous SSc (dcSSc) and 3 controls were analyzed for SDF-1 and CXCR4 by confocal laser scanning microscopy, RT-PCR, and Western blotting. Results SDF-1 and CXCR4 were up-regulated in the skin of patients with early (edematous) SSc, both in the diffuse and limited cutaneous forms, and progressively decreased, with the lowest expression in the latest phases of both SSc subsets. MVECs from patients with dcSSc expressed significantly higher amounts of both isoforms of SDF-1 in the early stage of disease, with a progressive reduction of SDF-1 and CXCR4 in later stages. On the surface of cultured MVECs from patients with dcSSc, SDF-1 and CXCR4 colocalized in polarized areas, suggesting that they are activated in vivo and that they are under strict genetic control to retain capping function. Conclusion Due to its transient expression, SDF-1 could be considered a future therapeutic target to induce new vessel formation in SSc. [source] Angiogenesis in patients with craniopharyngiomasCANCER, Issue 3 2002Correlation with treatment, outcome Abstract BACKGROUND Craniopharyngiomas are histologically benign epithelial neoplasms of the sellar region that often exhibit aggressive and invasive growth. The authors hypothesized that tumor proliferation, spread, and recurrence are angiogenesis dependent and investigated the significance of vascularization relative to biologic behavior. To the authors' knowledge, angiogenesis for patients with craniopharyngiomas has not been examined to date. METHODS The authors measured microvessel densities in resected, histologically proven craniopharyngiomas using immunostains for CD-34, a monoclonal antibody that selectively recognizes endothelial cells. Both histologic types of craniopharyngiomas, adamantinomatous and papillary, were included in the study. In addition, the cellular distribution of vascular endothelial growth factor (VEGF), a strong stimulator of new vessel formation, was assessed by both immunohistochemistry and in situ hybridization for VEGF receptor 2 (VEGFR-2) mRNA expression. RESULTS Histologically, small numbers of capillaries were identified in temporal stroma but not in their epithelial components. Immunohistochemistry revealed strong, conclusive cytoplasmic immunoreactivity for VEGF in the epithelial cells of both adamantinomatous craniopharyngiomas and papillary craniopharyngiomas. In situ hybridization showed that VEGFR-2 mRNA was expressed widely, not only in neoplastic epithelium but also in capillary endothelium. CONCLUSIONS Tumors with greater microvessel density regrow more frequently compared with tumors that have lower microvessel density, suggesting that the extent of angiogenesis is of prognostic value in patients with craniopharyngioma. VEGFR-2 may act as a key modulator of VEGF activity in endothelial cells and nonendothelial cells, indicating that VEGF plays an important role in the behavior of craniopharyngiomas. Cancer 2002;94:738,45. © 2002 American Cancer Society. DOI 10.1002/cncr.10281 [source] 3121: Oxygen and treatment of ocular ischemic diseasesACTA OPHTHALMOLOGICA, Issue 2010E STEFANSSON Purpose In ischemia, reduced blood flow results in hypoxia. Hypoxic cells make hypoxia inducible factor (HIF), which controls many of the adaptive responses of tissue to ischemia. This includes vasodilatation, production of vascular endothelial factor (VEGF) with neovascularization and leakage, and finally apoptosis and tissue atrophy. Methods If hypoxia is improved this will reduce the production of VEGF and thereby reduce new vessel formation on one hand and vascular leakage and edeam formation on the other. Several methods are available to improve retinal hypoxia, including laser treatment, vitrectomy, vasodilatory drugs such as carbonic anhydrase inhibitors in addition to breathing oxygen. These treatment methods have been studied by many research groups with invasive polarographic electrodes and optical probes as well as noninvasive oxymetry in human patients and animal subjects. Results We will review experimental and clinical studies, which confirm that oxygen tension of the retina is increased following 1. retinal laser treatment 2. Vitrectomy 3. carbonic anhydrase inhibitors Conclusion Oxygen is the natural control of VEGF. VEGF levels in the retina and other ocular tissues are affected by oxygen levels and ischeimc diseases are currently treated with methods that affect oxygen and consequently VEGF. The addition of anti VEGF drugs to oxygen directed treatment such as laser and vitrectomy further influences the oxygen-HIF-VEGF-neovascularization/edema axis in ischemic retinopathies. [source] USE OF PORCINE SMALL INTESTINAL SUBMUCOSA IN BLADDER AUGMENTATION IN RABBIT: LONG-TERM HISTOLOGICAL OUTCOMEANZ JOURNAL OF SURGERY, Issue 1-2 2008Ali Ayyildiz Aim: To investigate long-term histological features of bladder augmentation using porcine small intestine submucosa (SIS) in a rabbit model. Materials and method: Sixteen New Zealand rabbits were used. Porcine SIS was provided by a manufactured formation derived from the pig. After partial cystectomy was carried out on the bladder, a single layer of SIS (Cook® -SIS Technology, Cook Biotech Incorporated, West Lafayette, IN, USA) (2 × 5 cm) was sewn to bladder with continuous 5/0 vicryl suture material in a watertight manner. Urinary diversion was not used. The rabbits were killed 12 months later and perivesical fat was removed together with bladder. The 5-,m preparations taken from the samples were stained with haematoxylin,eosin and Mason's trichrome dye. S-100 and F8 stains were also used for immunohistochemical investigations. Results: The macroscopic view of bladder was normal. SIS was indistinguishable from normal bladder wall, but the region of the graft had a slight white coloration. Microscopic observations showed the continuity of transitional epithelium of host bladder tissue on SIS material. Detrusor and serosal layers were formed and these layers were indistinguishable from host bladder. Fibroblasts were scattered among the collagen fibrils. New vessel formations were present without lymphatic proliferation. Nerve regeneration was excellent. No inflammation was observed in normal and regenerated bladder wall. Conclusion: At the end of 12 months, the long-term histological features of bladder augmentation with porcine SIS in a rabbit model, such as presence of new vessel formations, nerve regeneration, collagen and smooth muscle regenerations, which were indistinguishable from original bladder, and the absence of inflammation, showed that SIS seems to be a viable alternative to the use of intestine in bladder augmentation. [source] | ||||||||||