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Results for “Neovascularization, Pathologic”

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At least 811 records · Page 45Linked to original sources
PubMed2004

Vascular remodeling in the circulations of the lung.

The lung is unique in its double sources of perfusion from the pulmonary and systemic circulations. One striking difference between the two circulations is the capacity for angiogenesis. The bronchial circulation has a capacity that seems quite similar to all systemic arteries, whereas the pulmonary circulation seems relatively inert in this regard. Extra-alveolar pulmonary arteries can grow somewhat in length, and septal capillaries seem to have the capability of reforming, but these processes do not seem to occur with nearly the same intensity associated with the bronchial arteries. In this review, we emphasize these differences between the two circulations of the lung, anticipating that future research will allow more focused probing into the molecular signaling that regulates the novel mechanistic and pathological pathways of each.

Animals↗
PubMed1990

Development of angiogenesis inhibitors for clinical applications.

Angiogenesis, the development of new blood vessels, is associated with many life-threatening pathologies. The neovascularization of tumors for example, allows a blood supply to deliver the required nutrients for tumor development. Inappropriate blood vessel growth also contributes to the pathology of other diseases such as atherosclerosis and arthritis. The process of angiogenesis is beginning to be better understood, and as Ted Maione and Richard Sharpe explain, this understanding has led to the identification of several lead compounds that inhibit this process. At present all of these candidate drugs exhibit severe host toxicity, but more selective angiogenesis inhibitors might be expected to be extremely useful therapeutic agents.

Animals↗
PubMedDate not supplied

Ocular neovascularization: an epidemiologic review.

Neovascularization occurs in many eye diseases, and its epidemiologic impact is significant. However, data on the prevalence and incidence of ocular neovascularization have never been compiled to demonstrate its pervasiveness. This overview of ocular angiogenesis provides a review of the epidemiologic literature for neovascularization in various parts of the eye, including the cornea, iris, retina, and choroid. Relevant disease states are reviewed, as are their risk factors, so that their pathogenesis can be better understood. Data on the prevalence and incidence of the major diseases involving angiogenesis are synthesized to provide statistical evidence of the span and magnitude of ocular neovascularization. These prevalence and incidence data on ocular neovascularization are extrapolated to USA population data where possible, and "worst-case" estimates are calculated as well. Information was gathered with a search of the MEDLINE database, published monographs and volumes, and consultation with a number of primary authors. This study attempts to unify much of past and present epidemiologic research, and the information is presented in sections divided according to the anatomy of the eye.

Choroid↗
PubMedDate not supplied

Retinal endothelial angiogenic activity: effects of hypoxia and glial (Müller) cells.

OBJECTIVE: To explore the impact of retinal glial (Müller) cells on survival and neovascularization-related activities of cultured retinal endothelial cells under normoxic and hypoxic conditions. METHODS: Bovine retinal endothelial cells (BRECs) were cultured under normoxia or hypoxia (0.5% O2) either alone, together with the human Müller cell line MIO-M1, or in normoxia- or hypoxia-conditioned media of MIO-M1 cells. Cell number, proliferation, apoptotic cell death, and migration of BRECs were determined. RESULTS: Exposure of BRECs to hypoxia for 24 h decreased the number of adherent cells and the proliferation rate, but increased apoptosis and cell migration. Increased apoptosis and decreased proliferation of the BRECs occurred also in the presence of conditioned media of MIO-M1 cells. Under normoxic conditions, co-culture with MIO-M1 cells resulted in increased proliferation, but decreased apoptosis and migration rates of BRECs. Under hypoxic conditions, the Müller cells released elevated amounts of VEGF but their presence decreased proliferation, apoptosis and the migration rates of BRECs. CONCLUSIONS: Hypoxia inhibits the proliferation of retinal endothelial cells. Müller cells release soluble mediators that enhance this hypoxia-mediated effect but, under certain conditions (i.e., in co-culture), may protect retinal endothelial cells from apoptosis, thus supporting their survival. Altogether the findings indicate that the key signal necessary to trigger retinal endothelial proliferation under hypoxia remains to be determined.

Animals↗
PubMed2005

[Peroxisome proliferator activated receptor ligands and angiogenesis].

PPAR receptors are expressed in endothelial cells and PPARalpha and gamma ligands play potent roles in modulating angiogenesis. Angiogenesis, the formation of new capillary blood vessels, is essential for many physiologic and pathologic processes such as cancer, choroidal neovascularization and ischemic diseases. Inhibition of angiogenesis can prevent diseases with excessive vessel growth such as cancer or diabetic retinopathy. Vascular endothelial growth factor (VEGF) and VEGF-receptors are considered key regulators of angiogenesis. PPARalpha and gamma ligands not only inhibit VEGF-receptor 2 expression but also act as blocker of VEGF-receptor signaling. Antiangiogenic action through targeting of VEGF-receptors may be a new approach to blocking hypoxia-driven angiogenesis. In this review, I highlight data concerning PPARs ligands involved in the biological mechanisms underlying antiangiogenesis.

Animals↗
PubMed2005

[Remodel retinal neovascularization by overexpression of HESR-1 in vitro].

OBJECTIVE: To remodel retinal neovascularization by overexpression of HESR-1 in vitro. METHODS: Human retinal capillary endothelial cell (HRCEC) was isolated, then HRCECs were transfected with pcDNA3.1+HESR-1. The changes of expression of KDR and occluding in HRCECs were analyzed using ELISA assay, the regulation of occluding in HRCECs by HESR-1 was evaluated by western blot. RESULTS: Over-expression of HESR-1 down-regulated KDR expression, but occludin expression was up-regulated in HRECEs, the result also showed that the vessels permeability was reduced by HESR-1. CONCLUSIONS: Overexpression of HESR-1 in HRCECs can inhibit the neovascularization and decrease the permeability of new vessels. It may be a promising gene therapy for intraocular neovascularization.

Basic Helix-Loop-Helix Proteins↗
PubMed1998

Indocyanine green angiography. American Academy of Ophthalmology.

The purpose of the Committee on Ophthalmic Procedures Assessment is to evaluate on a scientific basis new and existing ophthalmic tests, devices, and procedures for their safety, efficacy, clinical effectiveness, and appropriate uses. Evaluations include examination of available literature, epidemiological analyses when appropriate, and compilation of opinions from recognized experts and other interested parties. After appropriate review by all contributors, including legal counsel, assessments are submitted to the Academy's Board of Trustees for consideration as official Academy policy.

Choroid↗
PubMed2001

Estrogen and angiogenesis: A review.

Multiple lines of evidence suggest that estrogen directly modulates angiogenesis via effects on endothelial cells. Under physiological conditions, angiogenesis is routinely observed in the uterus in association with fluctuations in the levels of circulating estradiol and other sex steroids. In pathological circumstances, such as breast cancer, a clear association between estrogen, estrogen receptor expression by endothelial cells, angiogenic activity, and/or tumor invasiveness has been made. Studies performed in our laboratory have revealed that estradiol accelerates functional endothelial recovery after arterial injury. Despite these consistent observations, the mechanisms by which estrogen regulates angiogenesis under physiological and pathological circumstances have not been defined.

Animals↗
PubMed2004

Endometrial angiogenesis: from physiology to pathology.

Numerous factors have been implicated in angiogenesis. This article concentrates on the expression of the major angiogenic factors, namely, vascular endothelial growth factor (VEGF) and the angiopoietins in the human endometrium. Particular emphasis is placed on the expression of the angiopoietins and their physiological and pathological expression.

Adenocarcinoma↗
PubMed2002

[Angiogenesis, anti-angiogenesis, and tumor suppression].

Recent studies have revealed that a number of gene products such as vascular endothelial growth factor and its receptors are deeply involved in the process of angiogenesis. Most of these genes were characterized not only by the biochemical/molecular biological approach but also by the genetical approach including the use of gene-targeted mice. Furthermore, some of these genes are strongly correlated with the formation of pathological blood vessels such as tumor angiogenesis, suggesting that these gene products are good candidates for screening anti-angiogenic materials. Inhibitors against VEGF and its receptors have been most extensively studied and developed, but inhibitors to other factors such as MMPs and angiopoietins may also be useful for developing anti-angiogenic materials. In addition to these molecules, unidentified gene products could be specifically involved in certain types of pathological angiogenesis.

Animals↗
PubMed2005

Regulation of lymphangiogenesis--from cell fate determination to vessel remodeling.

Lymphatic vessels are important for the maintenance of normal tissue fluid balance, immune surveillance and adsorption of digested fats. During the past decade, the identification of lymphatic-specific markers and growth factors has enabled detailed studies of the lymphatic system, and gain- and loss-of-function experiments have greatly increased our understanding of the mechanisms of normal lymphatic development. Understanding the basic biology has provided novel insights into the pathologic conditions of the lymphatic system that contribute to lymphedema, inflammation or lymphatic metastasis, and opened possibilities for the development of better therapeutic strategies. Here we review the current knowledge about the molecular mechanisms regulating the development of the lymphatic vasculature; of the differentiation of lymphatic endothelial cells, of the regulation of the growth of lymphatic vessels, and of remodeling of the vasculature into a network consisting of lymphatic capillaries and collecting lymphatic vessels. Furthermore, we will discuss the molecular mechanisms involved in the pathological conditions of the lymphatic vessels.

Angiopoietins↗
PubMed2000

Mechanisms of angiogenesis and arteriogenesis.

Endothelial and smooth muscle cells interact with each other to form new blood vessels. In this review, the cellular and molecular mechanisms underlying the formation of endothelium-lined channels (angiogenesis) and their maturation via recruitment of smooth muscle cells (arteriogenesis) during physiological and pathological conditions are summarized, alongside with possible therapeutic applications.

Animals↗
PubMedDate not supplied

Correlation between angiographic and pathological findings in experimental choroidal neovascular membranes after transpupillary thermotherapy.

PURPOSE: To evaluate the correlation between angiographic and pathological findings in experimental choroidal neovascular membranes after transpupillary thermotherapy (TTT). METHODS: Experimental subretinal choroidal neovascular membranes were produced in the monkey eye macula by intense photocoagulation. TTT was delivered, targeting the choroidal neovascular membranes, using a diode laser at 810 nm. One week and 4 weeks after TTT, indocyanine green angiography (IA), fluorescein angiography (FA), optical coherence tomography (OCT), and histological examinations were performed. RESULTS: One week after TTT, indocyanine green dye leakage from choroidal neovascular membranes was reduced on IA, and FA showed staining in the late phase. Light microscopic examination showed numerous small-caliber blood vessels and persistent subretinal exudation. Four weeks after TTT, there was no indocyanine green dye leakage on IA, and FA showed staining. OCT showed a decrease in retinal detachment. Light microscopic examination showed fewer blood vessels and subretinal exudation had disappeared. Choroidal neovascular membranes were composed of fibrous tissue. CONCLUSIONS: Changes in angiographic and OCT findings observed after TTT were inferred to be the result of accelerated fibrosis due to TTT and the disappearance of exudation.

Animals↗
PubMed1989

Endothelium-fibrinolysis system interaction.

The role of urokinase-type plasminogen activator (u-PA) in capillary growth was investigated using cultured bovine endothelial cells (BCE) on type I collagen gels and analyzed by morphometry for quantitative assessment of angiogenesis in vitro. BCE migrated into the gel matrix and formed capillary-like networks. The morphometrical analyses by measuring the length of tube formation enabled us to evaluate the effects of fibrinolytic proteases and several reagents. The addition of plasminogen up to 25 micrograms/ml to the gels significantly increased the extent of tube formation of BCE in a dose-dependent manner. Basic fibroblast growth factor (10 ng/ml) increased tube formation only in the presence of plasminogen. These enhancing effects on angiogenesis appeared to be related to the activation of fibrinolysis by u-PA derived from BCE, because they were suppressed by the addition of anti-u-PA IgG and anti-plasmin reagents such as aprotinin and alpha 2 anti-plasmin. Transforming growth factor beta also enhanced tube formation of BCE, but tumor necrosis factor alpha and interleukin-1 suppressed the tube formation. The quantitative assay of angiogenesis may be useful for clarifying the mechanism of neovascularization under pathological conditions.

Animals↗
PubMed2003

Erythropoietin as an angiogenic factor.

Erythropoietin (Epo) is produced by the fetal liver and adult kidney and is an essential stimulator of erythropoiesis. It has, however, been shown to modulate host cellular signal transduction pathway to perform many other functions. New sites of Epo production have been found, such as the female reproductive organs and central nervous system. This review summarizes the involvement of Epo in the regulation of angiogenesis in both normal and pathological conditions.

Angiogenesis Inducing Agents↗
PubMed1996

Pericytes in the microvasculature.

Pericytes, also known as Rouget cells or mural cells, are associated abluminally with all vascular capillaries and post-capillary venules. Differences in pericyte morphology and distribution among vascular beds suggest tissue-specific functions. Based on their location and their complement of muscle cytoskeletal proteins, pericytes have been proposed to play a role in the regulation of blood flow. In vitro studies demonstrating the contractile ability of pericytes support this concept. Pericytes have also been suggested to be oligopotential and have been reported to differentiate into adipocytes, osteoblasts and phagocytes. The mechanisms involved in vessel formation have yet to be elucidated but observations indicate that the primordial endothelium can recruit undifferentiated mesenchymal cells and direct their differentiation into pericytes in microvessels, and smooth muscle cells in large vessels. Communication between endothelial cells and pericytes, or their precursors, may take many forms. Soluble factors such as platelet-derived growth factor and transforming growth factors-beta are likely to be involved. In addition, physical contact mediated by cell adhesion molecules, integrins and gap junctions appear to contribute to the control of vascular growth and function. Development of culture methods has allowed some functions of pericytes to be directly examined. Co-culture of pericytes with endothelial cells leads to the activation of transforming growth factor-beta, which in turn influences the growth and differentiation of the vascular cells. Finally, the pericyte has been implicated in the development of a variety of pathologies including hypertension, multiple sclerosis, diabetic microangiopathy and tumor vascularization.

Animals↗
PubMed1996

Vascular endothelial growth factor and its receptors.

Vascular endothelial growth factor (VEGF) is a prime regulator of endothelial cell proliferation, angiogenesis, vasculogenesis and vascular permeability. Its activity is mediated by the high affinity tyrosine kinase receptors, KDR/Fik-1 and Fit-1. In this article, recently discovered structural, molecular and biological properties of VEGF are described. Among the topics discussed are VEGF and VEGF receptor structure and bioactivity, the regulation of VEGF expression, the role of VEGF and its receptors in vascular development, and the involvement of VEGF and its receptors in normal and pathological (ocular and tumor) angiogenesis.

Animals↗