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    820 results match your criteria Angiogenesis [Journal]

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    A xenograft model for venous malformation.
    Angiogenesis 2018 May 21. Epub 2018 May 21.
    Division of Experimental Hematology and Cancer Biology, Cancer and Blood Diseases Institute, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, 45229-3039, USA.
    Vascular malformations are defects caused by the abnormal growth of the vasculature. Among them, venous malformation (VM) is an anomaly characterized by slow-flow vascular lesions with abnormally shaped veins, typically in sponge-like configuration. VMs can expand over years causing disfigurement, obstruction of vital structures, thrombosis, bleeding, and pain. Read More

    Preclinical impact of high dose intermittent antiangiogenic tyrosine kinase inhibitor pazopanib in intrinsically resistant tumor models.
    Angiogenesis 2018 May 21. Epub 2018 May 21.
    Department of Medical Biophysics, University of Toronto, Toronto, ON, M5S 2J7, Canada.
    Antiangiogenic tyrosine kinase inhibitors (TKIs) target vascular endothelial growth factor receptors and other receptor tyrosine kinases. As a result of toxicity, the clinical failures or the modest benefits associated with antiangiogenic TKI therapy may be related in some cases to suboptimal drug dosing and scheduling, thereby facilitating resistance. Most antiangiogenic TKIs, including pazopanib, are administered on a continuous daily basis. Read More

    Improved recovery from limb ischaemia by delivery of an affinity-isolated heparan sulphate.
    Angiogenesis 2018 May 18. Epub 2018 May 18.
    Glycotherapeutics Group, Institute of Medical Biology, Agency for Science, Technology and Research, 8A Biomedical Grove, Immunos #06-06, Singapore, 138648, Singapore.
    Peripheral arterial disease is a major cause of limb loss and its prevalence is increasing worldwide. As most standard-of-care therapies yield only unsatisfactory outcomes, more options are needed. Recent cell- and molecular-based therapies that have aimed to modulate vascular endothelial growth factor-165 (VEGF) levels have not yet been approved for clinical use due to their uncertain side effects. Read More

    Consensus guidelines for the use and interpretation of angiogenesis assays.
    Angiogenesis 2018 May 15. Epub 2018 May 15.
    Angiogenesis Laboratory, Department of Medical Oncology, VU University Medical Center, Cancer Center Amsterdam, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands.
    The formation of new blood vessels, or angiogenesis, is a complex process that plays important roles in growth and development, tissue and organ regeneration, as well as numerous pathological conditions. Angiogenesis undergoes multiple discrete steps that can be individually evaluated and quantified by a large number of bioassays. These independent assessments hold advantages but also have limitations. Read More

    Targeting glioblastoma-derived pericytes improves chemotherapeutic outcome.
    Angiogenesis 2018 May 14. Epub 2018 May 14.
    Department of Pathology, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil.
    Glioblastoma is the most common malignant brain cancer in adults, with poor prognosis. The blood-brain barrier limits the arrival of several promising anti-glioblastoma drugs, and restricts the design of efficient therapies. Recently, by using state-of-the-art technologies, including thymidine kinase targeting system in combination with glioblastoma xenograft mouse models, it was revealed that targeting glioblastoma-derived pericytes improves chemotherapy efficiency. Read More

    Correction to: Soluble delta-like 1 homolog (DLK1) stimulates angiogenesis through Notch1/Akt/eNOS signaling in endothelial cells.
    Angiogenesis 2018 May 10. Epub 2018 May 10.
    Center for Neuroscience, National Sun Yat-Sen University, Kaohsiung, Taiwan.
    In the original publication of the article, there is an error in one of the citations in the Discussion section. Read More

    eNOS expression and NO release during hypoxia is inhibited by miR-200b in human endothelial cells.
    Angiogenesis 2018 May 8. Epub 2018 May 8.
    Department of Biology and Pharmaceutical Botany, Medical University of Gdansk, Hallera 107, 80-416, Gdańsk, Poland.
    The nitric oxide (NO) secreted by vascular endothelium is required for the maintenance of cardiovascular homeostasis. Diminished release of NO generated by endothelial NO synthase contributes to endothelial dysfunction. Hypoxia and ischemia reduce endothelial eNOS expression via posttranscriptional mechanisms that result in NOS3 transcript destabilization. Read More

    Gene therapy knockdown of VEGFR2 in retinal endothelial cells to treat retinopathy.
    Angiogenesis 2018 May 5. Epub 2018 May 5.
    John A. Moran Eye Center, University of Utah, 65 N. Mario Capecchi Drive, Salt Lake City, UT, 84132, USA.
    Inhibition of vascular endothelial growth factor (VEGF) in retinopathy of prematurity (ROP) raises concerns for premature infants because VEGF is essential for retinovascular development as well as neuronal and glial health. This study tested the hypothesis that endothelial cell-specific knockdown of VEGF receptor 2 (VEGFR2), or downstream STAT3, would inhibit VEGF-induced retinopathy without delaying physiologic retinal vascular development. We developed an endothelial cell-specific lentiviral vector that delivered shRNAs to VEGFR2 or STAT3 and a green fluorescent protein reporter under control of the VE-cadherin promoter. Read More

    Assessment of the direct effects of DDAH I on tumour angiogenesis in vivo.
    Angiogenesis 2018 May 2. Epub 2018 May 2.
    Molecular and Clinical Sciences Research Institute, St. George's, University of London, Cranmer Terrace, London, SW17 0RE, UK.
    Nitric oxide (NO) has been strongly implicated in glioma progression and angiogenesis. The endogenous inhibitors of NO synthesis, asymmetric dimethylarginine (ADMA) and N-monomethyl-L-arginine (L-NMMA), are metabolized by dimethylarginine dimethylaminohydrolase (DDAH), and hence, DDAH is an intracellular factor that regulates NO. However, DDAH may also have an NO-independent action. Read More

    Angio-3, a 10-residue peptide derived from human plasminogen kringle 3, suppresses tumor growth in mice via impeding both angiogenesis and vascular permeability.
    Angiogenesis 2018 Apr 24. Epub 2018 Apr 24.
    Department of Biological Sciences, Faculty of Science, National University of Singapore, Singapore, 117543, Singapore.
    Anti-angiogenesis therapy is an established therapeutic strategy for cancer. The endogenous angiogenic inhibitor angiostatin contains the first 3-4 kringle domains of plasminogen and inhibits both angiogenesis and vascular permeability. We present here a 10-residue peptide, Angio-3, derived from plasminogen kringle 3, which retains the functions of angiostatin in inhibiting both angiogenesis and vascular permeability. Read More

    SNAI1, an endothelial-mesenchymal transition transcription factor, promotes the early phase of ocular neovascularization.
    Angiogenesis 2018 Apr 19. Epub 2018 Apr 19.
    Department of Ophthalmology, Eye Institute of Chinese PLA, Xijing Hospital, Fourth Military Medical University, Xi'an, 710032, China.
    Ocular neovascularization is a comprehensive process involved in retinal vascular development and several blinding diseases such as age-related macular degeneration and retinopathy of prematurity, with vascular endothelial growth factor (VEGF) regarded as the master regulator. However, the qualified effect of anti-VEGF therapy reveals that the underlying mechanisms are still not clearly identified. To initialize angiogenesis, endothelial cells undergo a phenotype switching to generate highly migratory and invasive cells. Read More

    Spatiotemporal heterogeneity and patterning of developing renal blood vessels.
    Angiogenesis 2018 Apr 7. Epub 2018 Apr 7.
    Department of Molecular Biology, Center for Regenerative Science and Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., NA8.300, Dallas, TX, 75390-9148, USA.
    The kidney vasculature facilitates the excretion of wastes, the dissemination of hormones, and the regulation of blood chemistry. To carry out these diverse functions, the vasculature is regionalized within the kidney and along the nephron. However, when and how endothelial regionalization occurs remains unknown. Read More

    BI1 is associated with microvascular protection in cardiac ischemia reperfusion injury via repressing Syk-Nox2-Drp1-mitochondrial fission pathways.
    Angiogenesis 2018 Apr 6. Epub 2018 Apr 6.
    Chinese PLA General Hospital, Medical School of Chinese PLA, Beijing, 100853, China.
    Background: Mitochondrial fission has been identified as the pathogenesis underlying the development of cardiac microvascular ischemia reperfusion (IR) injury, although the regulatory signaling upstream from fission is far from clear. Bax inhibitor is a novel anti-apoptotic factor, and, however, its role of cardiac microvascular IR injury and mitochondrial homeostasis remains unclear.

    Methods: The cardiac microvascular IR injury was performed in WT mice and BI1 transgenic (BI ) mice. Read More

    Characterization of isolated liver sinusoidal endothelial cells for liver bioengineering.
    Angiogenesis 2018 Mar 26. Epub 2018 Mar 26.
    O'Brien Institute Department, St Vincent's Institute of Medical Research, Melbourne, Australia.
    Background: The liver sinusoidal capillaries play a pivotal role in liver regeneration, suggesting they may be beneficial in liver bioengineering. This study isolated mouse liver sinusoidal endothelial cells (LSECs) and determined their ability to form capillary networks in vitro and in vivo for liver tissue engineering purposes.

    Methods And Results: In vitro LSECs were isolated from adult C57BL/6 mouse livers. Read More

    Extracellular vesicle-carried Jagged-1 inhibits HUVEC sprouting in a 3D microenvironment.
    Angiogenesis 2018 Mar 14. Epub 2018 Mar 14.
    Department of Biological Sciences, National University of Singapore, Singapore, 117543, Singapore.
    NOTCH signalling is an evolutionarily conserved juxtacrine signalling pathway that is essential in development. Jagged1 (JAG1) and Delta-like ligand 4 (DLL4) are transmembrane NOTCH ligands that regulate angiogenesis by controlling endothelial cell (EC) differentiation, vascular development and maturation. In addition, DLL4 could bypass its canonical cell-cell contact-dependent signalling to influence NOTCH signalling and angiogenesis at a distance when it is packaged into extracellular vesicles (EVs). Read More

    Platelet function is disturbed by the angiogenesis inhibitors sunitinib and sorafenib, but unaffected by bevacizumab.
    Angiogenesis 2018 May 12;21(2):325-334. Epub 2018 Mar 12.
    Department of Medical Oncology, Cancer Center Amsterdam, VU University Medical Center, De Boelelaan, 1117, 1081 HV, Amsterdam, The Netherlands.
    Introduction: At the clinical introduction of antiangiogenic agents as anticancer agents, no major toxicities were expected as merely just endothelial cells (ECs) in tumors would be affected. However, several (serious) toxicities became apparent, of which underlying mechanisms are largely unknown. We investigated to what extent sunitinib (multitargeted antiangiogenic tyrosine kinase inhibitor (TKI)), sorafenib (TKI) and bevacizumab [specific antibody against vascular endothelial growth factor (VEGF)] may impair platelet function, which might explain treatment-related bleedings. Read More

    Peripheral post-ischemic vascular repair is impaired in a murine model of Alzheimer's disease.
    Angiogenesis 2018 Mar 7. Epub 2018 Mar 7.
    Institut des Vaisseaux et du Sang, 8 rue Guy Patin, 75475, Paris Cedex 10, France.
    The pathophysiology of sporadic Alzheimer's disease (AD) remains uncertain. Along with brain amyloid-β (Aβ) deposits and neurofibrillary tangles, cerebrovascular dysfunction is increasingly recognized as fundamental to the pathogenesis of AD. Using an experimental model of limb ischemia in transgenic APPPS1 mice, a model of AD (AD mice), we showed that microvascular impairment also extends to the peripheral vasculature in AD. Read More

    Characterization of a drug-targetable allosteric site regulating vascular endothelial growth factor signaling.
    Angiogenesis 2018 Mar 3. Epub 2018 Mar 3.
    Laboratory of Biomolecular Research, Paul Scherrer Institut, 5232, Villigen, Switzerland.
    Vascular endothelial growth factors (VEGFs) regulate blood and lymph vessel development upon activation of three receptor tyrosine kinases (VEGFRs). The extracellular domain of VEGFRs consists of seven Ig-homology domains, of which D2-3 form the ligand-binding site, while the membrane proximal domains D4-7 are involved in homotypic interactions in ligand-bound receptor dimers. Based on low-resolution structures, we identified allosteric sites in D4-5 and D7 of vascular endothelial growth factor receptor 2 (VEGFR-2) accomplishing regulatory functions. Read More

    Different angioregulatory activity of monovalent galectin-9 isoforms.
    Angiogenesis 2018 Mar 2. Epub 2018 Mar 2.
    Angiogenesis Laboratory, Department of Medical Oncology, Cancer Center Amsterdam, VU University Medical Center, De Boelelaan 1118, 1081 HV, Amsterdam, The Netherlands.
    Galectin-9 consists of two peptide-linked carbohydrate recognition domains (CRDs), but alternative splicing and proteolytic processing can give rise to multiple galectin-9 isoforms. Some of these consist of a single CRD and can exert different functions in cell biology. Here, we explored the role of these galectin-9 isoforms in endothelial cell function and angiogenesis. Read More

    Serum/glucocorticoid-regulated kinase 1 as a novel transcriptional target of bone morphogenetic protein-ALK1 receptor signaling in vascular endothelial cells.
    Angiogenesis 2018 May 24;21(2):415-423. Epub 2018 Feb 24.
    Department of Molecular Physiology, National Cerebral and Cardiovascular Center Research Institute, 5-7-1 Fujishiro-dai, Suita, Osaka, 565-8565, Japan.
    Bone morphogenetic protein 9 (BMP9)/BMP10-ALK1 receptor signaling is essential for endothelial differentiation and vascular morphogenesis. Mutations in ALK1/ACVRL1 and other signal-related genes are implicated in human vascular diseases, and the Alk1/Acvrl1 deletion in mice causes severe impairment of vascular formation and embryonic lethality. In the microarray screen to search for novel downstream genes of ALK1 signaling, we found that the mRNA and protein expression of serum/glucocorticoid-regulated kinase 1 (SGK1) was rapidly up-regulated by the BMP9 stimulation of cultured human endothelial cells. Read More

    Vascular deficiency of Smad4 causes arteriovenous malformations: a mouse model of Hereditary Hemorrhagic Telangiectasia.
    Angiogenesis 2018 May 19;21(2):363-380. Epub 2018 Feb 19.
    Cell and Molecular Biology Department, Tulane University, New Orleans, LA, 70118, USA.
    Hereditary hemorrhagic telangiectasia (HHT) is an autosomal dominant vascular disorder that leads to abnormal connections between arteries and veins termed arteriovenous malformations (AVM). Mutations in TGFβ pathway members ALK1, ENG and SMAD4 lead to HHT. However, a Smad4 mouse model of HHT does not currently exist. Read More

    High-density lipoprotein (HDL) promotes angiogenesis via S1P3-dependent VEGFR2 activation.
    Angiogenesis 2018 May 15;21(2):381-394. Epub 2018 Feb 15.
    Department of Neurology, University Hospital Essen, Hufelandstrasse 55, 45122, Essen, Germany.
    High-density lipoprotein (HDL) has previously been shown to promote angiogenesis. However, the mechanisms by which HDL enhances the formation of blood vessels remain to be defined. To address this, the effects of HDL on the proliferation, transwell migration and tube formation of human umbilical vein endothelial cells were investigated. Read More

    Time-dependent LXR/RXR pathway modulation characterizes capillary remodeling in inflammatory corneal neovascularization.
    Angiogenesis 2018 May 14;21(2):395-413. Epub 2018 Feb 14.
    Department of Ophthalmology, Faculty of Health Sciences, Institute for Clinical and Experimental Medicine, Linkoping University, 58183, Linköping, Sweden.
    Inflammation in the normally immune-privileged cornea can initiate a pathologic angiogenic response causing vision-threatening corneal neovascularization. Inflammatory pathways, however, are numerous, complex and are activated in a time-dependent manner. Effective resolution of inflammation and associated angiogenesis in the cornea requires knowledge of these pathways and their time dependence, which has, to date, remained largely unexplored. Read More

    Visualization of endothelial cell cycle dynamics in mouse using the Flt-1/eGFP-anillin system.
    Angiogenesis 2018 May 7;21(2):349-361. Epub 2018 Feb 7.
    Institute of Physiology I, Life and Brain Center, Medical Faculty, University of Bonn, Sigmund-Freud-Str. 25, 53127, Bonn, Germany.
    Endothelial cell proliferation is a key process during vascular growth but its kinetics could only be assessed in vitro or ex vivo so far. To enable the monitoring and quantification of cell cycle kinetics in vivo, we have generated transgenic mice expressing an eGFP-anillin construct under control of the endothelial-specific Flt-1 promoter. This construct labels the nuclei of endothelial cells in late G1, S and G2 phase and changes its localization during the different stages of M phase, thereby enabling the monitoring of EC proliferation and cytokinesis. Read More

    Glomerular endothelial cell maturation depends on ADAM10, a key regulator of Notch signaling.
    Angiogenesis 2018 May 3;21(2):335-347. Epub 2018 Feb 3.
    Department of Physiology, Biophysics and Systems Biology, Weill Cornell Medicine, New York, NY, USA.
    The principal function of glomeruli is to filter blood through a highly specialized filtration barrier consisting of a fenestrated endothelium, the glomerular basement membrane and podocyte foot processes. Previous studies have uncovered a crucial role of endothelial a disintegrin and metalloprotease 10 (ADAM10) and Notch signaling in the development of glomeruli, yet the resulting defects have not been further characterized nor understood in the context of kidney development. Here, we used several different experimental approaches to analyze the kidneys and glomeruli from mice lacking ADAM10 in endothelial cells (A10ΔEC mice). Read More

    Somatic NRAS mutation in patient with generalized lymphatic anomaly.
    Angiogenesis 2018 May 3;21(2):287-298. Epub 2018 Feb 3.
    Department of Dermatology, Sheba Medical Center, Tel Hashomer, Ramat Gan, Israel.
    Generalized lymphatic anomaly (GLA or lymphangiomatosis) is a rare disease characterized by a diffuse proliferation of lymphatic vessels in skin and internal organs. It often leads to progressive respiratory failure and death, but its etiology is unknown. Here, we isolated lymphangiomatosis endothelial cells from GLA tissue. Read More

    miRNAs regulate the HIF switch during hypoxia: a novel therapeutic target.
    Angiogenesis 2018 May 27;21(2):183-202. Epub 2018 Jan 27.
    Department of Biology and Pharmaceutical Botany, Medical University of Gdansk, Hallera 107, 80-416, Gdańsk, Poland.
    The decline of oxygen tension in the tissues below the physiological demand leads to the hypoxic adaptive response. This physiological consequence enables cells to recover from this cellular insult. Understanding the cellular pathways that mediate recovery from hypoxia is therefore critical for developing novel therapeutic approaches for cardiovascular diseases and cancer. Read More

    Soluble delta-like 1 homolog (DLK1) stimulates angiogenesis through Notch1/Akt/eNOS signaling in endothelial cells.
    Angiogenesis 2018 May 30;21(2):299-312. Epub 2018 Jan 30.
    Center for Neuroscience, National Sun Yat-Sen University, Kaohsiung, Taiwan.
    Aim: Delta-like 1 homolog (DLK1) is a non-canonical ligand of Notch signaling, which plays a pivotal role in vascular development and tumor angiogenesis. This study aimed to elucidate the function and mechanism of DLK1 in angiogenesis.

    Methods And Results: By using in situ hybridization and immunohistochemical studies, expression analysis revealed a unique vascular tropism of DLK1 in vasculature of neuroblastoma and vascular tumors. Read More

    Direct repression of IGF2 is implicated in the anti-angiogenic function of microRNA-210 in human retinal endothelial cells.
    Angiogenesis 2018 May 15;21(2):313-323. Epub 2018 Jan 15.
    Yueyang Hospital and Clinical Research Institute of Integrative Medicine, Shanghai University of Traditional Chinese Medicine, 110 Ganhe Rd, Shanghai, 200437, China.
    Pathological angiogenesis leads to the development of retinal vasculopathies and causes severe vision impairment. Increased understanding of the mechanisms underlying the angiogenic behavior of retinal endothelial cells helps provide new insights for developing treatment of retinal vasculopathies. Pro-angiogenic function of miR-210 has previously been identified. Read More

    Selective IKK2 inhibitor IMD0354 disrupts NF-κB signaling to suppress corneal inflammation and angiogenesis.
    Angiogenesis 2018 May 13;21(2):267-285. Epub 2018 Jan 13.
    Department of Ophthalmology, Institute for Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, 58183, Linköping, Sweden.
    Corneal neovascularization is a sight-threatening condition caused by angiogenesis in the normally avascular cornea. Neovascularization of the cornea is often associated with an inflammatory response, thus targeting VEGF-A alone yields only a limited efficacy. The NF-κB signaling pathway plays important roles in inflammation and angiogenesis. Read More

    Oxidized phospholipids stimulate production of stem cell factor via NRF2-dependent mechanisms.
    Angiogenesis 2018 May 12;21(2):229-236. Epub 2018 Jan 12.
    Department of Pharmaceutical Chemistry, Institute of Pharmaceutical Sciences, University of Graz, Humboldtstrasse 46/III, 8010, Graz, Austria.
    Receptor tyrosine kinase c-Kit and its ligand stem cell factor (SCF) regulate resident vascular wall cells and recruit circulating progenitors. We tested whether SCF may be induced by oxidized palmitoyl-arachidonoyl-phosphatidylcholine (OxPAPC) known to accumulate in atherosclerotic vessels. Gene expression analysis demonstrated OxPAPC-induced upregulation of SCF mRNA and protein in different types of endothelial cells (ECs). Read More

    IL-11 facilitates a novel connection between RA joint fibroblasts and endothelial cells.
    Angiogenesis 2018 May 11;21(2):215-228. Epub 2018 Jan 11.
    Jesse Brown VA Medical Center, Chicago, IL, 60612, USA.
    IL-11 has been detected in inflamed joints; however, its role in the pathogenesis of arthritis is not yet clear. Studies were conducted to characterize the expression and functional significance of IL-11 and IL-11Rα in rheumatoid arthritis (RA). IL-11 levels were elevated in RA synovial fluid (SF) compared to osteoarthritis (OA) SF and plasma from RA, OA and normal individuals (NLs). Read More

    AAV-mediated gene delivery of the calreticulin anti-angiogenic domain inhibits ocular neovascularization.
    Angiogenesis 2018 Feb 9;21(1):95-109. Epub 2018 Jan 9.
    Department of Ophthalmology, The First Affiliated Hospital of Jinan University, Guangzhou, Guangdong, China.
    Ocular neovascularization is a common pathological feature in diabetic retinopathy and neovascular age-related macular degeneration that can lead to severe vision loss. We evaluated the therapeutic efficacy of a novel endogenous inhibitor of angiogenesis, the calreticulin anti-angiogenic domain (CAD180), and its functional 112-residue fragment, CAD-like peptide 112 (CAD112), delivered using a self-complementary adeno-associated virus serotype 2 (scAAV2) in rodent models of oxygen-induced retinopathy and laser-induced choroidal neovascularization. The expression of CAD180 and CAD112 was elevated in human umbilical vein endothelial cells transduced with scAAV2-CAD180 or scAAV2-CAD112, respectively, and both inhibited angiogenic activity in vitro. Read More

    Chronic mild hypoxia promotes profound vascular remodeling in spinal cord blood vessels, preferentially in white matter, via an α5β1 integrin-mediated mechanism.
    Angiogenesis 2018 May 3;21(2):251-266. Epub 2018 Jan 3.
    Department of Molecular Medicine, MEM-132, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA, 92037, USA.
    Spinal cord injury (SCI) leads to rapid destruction of neuronal tissue, resulting in devastating motor and sensory deficits. This is exacerbated by damage to spinal cord blood vessels and loss of vascular integrity. Thus, approaches that protect existing blood vessels or stimulate the growth of new blood vessels might present a novel approach to minimize loss or promote regeneration of spinal cord tissue following SCI. Read More

    Slit2/Robo1 signaling is involved in angiogenesis of glomerular endothelial cells exposed to a diabetic-like environment.
    Angiogenesis 2018 May 3;21(2):237-249. Epub 2018 Jan 3.
    Department of Nephrology, Xinqiao Hospital, Third Military Medical University, Chongqing, 400037, China.
    Abnormal angiogenesis plays a pathological role in diabetic nephropathy (DN), contributing to glomerular hypertrophy and microalbuminuria. Slit2/Robo1 signaling participates in angiogenesis in some pathological contexts, but whether it is involved in glomerular abnormal angiogenesis of early DN is unclear. The present study evaluated the effects of Slit2/Robo1 signaling pathway on angiogenesis of human renal glomerular endothelial cells (HRGECs) exposed to a diabetic-like environment or recombinant Slit2-N. Read More

    Tip-cell behavior is regulated by transcription factor FoxO1 under hypoxic conditions in developing mouse retinas.
    Angiogenesis 2018 May 28;21(2):203-214. Epub 2017 Nov 28.
    Kagawa Prefectural University of Health Sciences, Hara 281-1, Mure, Takamatsu, Kagawa, 761-0123, Japan.
    Forkhead box protein O1 (FoxO1) is a transcription factor and a critical regulator of angiogenesis. Various environmental stimuli, including growth factors, nutrients, shear stress, oxidative stress and hypoxia, affect FoxO1 subcellular localization and strongly influence its transcriptional activity; however, FoxO1-localization patterns in endothelial cells (ECs) during development have not been clarified in vivo. Here, we reported that FoxO1 expression was observed in three layers of angiogenic vessels in developing mouse retinas and that among these layers, the front layer showed high levels of FoxO1 expression in the nuclei of most tip ECs. Read More

    Dimethylarginine dimethylaminohydrolase-1 (DDAH1) is frequently upregulated in prostate cancer, and its overexpression conveys tumor growth and angiogenesis by metabolizing asymmetric dimethylarginine (ADMA).
    Angiogenesis 2018 Feb 17;21(1):79-94. Epub 2017 Nov 17.
    Center for Chemical Biology, CSIR-Indian Institute of Chemical Technology (CSIR-IICT), Tarnaka, Uppal Road, Hyderabad, 007, India.
    Tissue microarray analysis confirmed higher dimethylarginine dimethylaminohydrolase-1 (DDAH1) expression in prostate cancer (PCa) compared to benign and normal prostate tissues. DDAH1 regulates nitric oxide (NO) production by degrading endogenous nitric oxide synthase (NOS) inhibitor, asymmetric dimethylarginine (ADMA). This study examined whether DDAH1 has any physiological role in PCa progression. Read More

    Noninvasive induction of angiogenesis in tissues by external suction: sequential optimization for use in reconstructive surgery.
    Angiogenesis 2018 Feb 17;21(1):61-78. Epub 2017 Nov 17.
    Tissue Engineering and Wound Healing Laboratory, Department of Surgery, Division of Plastic Surgery, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, 02115, USA.
    In reconstructive surgery, tissues are routinely transferred to repair a defect caused by trauma, cancer, chronic diseases, or congenital malformations; surgical transfer intrinsically impairs metabolic supply to tissues placing a risk of ischemia-related complications such as necrosis, impaired healing, or infection. Pre-surgical induction of angiogenesis in tissues (preconditioning) can limit postsurgical ischemic complications and improve outcomes, but very few preconditioning strategies have successfully been translated to clinical practice due to the invasiveness of most proposed approaches, their suboptimal effects, and their challenging regulatory approval. We optimized a method that adopts noninvasive external suction to precondition tissues through the induction of hypoxia-mediated angiogenesis. Read More

    Executive summary of the 12th HHT international scientific conference.
    Angiogenesis 2018 Feb;21(1):169-181
    Department of Pulmonology, St. Antonius Hospital, Koekoekslaan 1, 3435 CM, Nieuwegein, The Netherlands.
    Hereditary hemorrhagic telangiectasia is an autosomal dominant trait affecting approximately 1 in 5000 people. A pathogenic DNA sequence variant in the ENG, ACVRL1 or SMAD4 genes, can be found in the majority of patients. The 12th International Scientific HHT Conference was held on June 8-11, 2017 in Dubrovnik, Croatia to present and discuss the latest scientific achievements, and was attended by over 200 scientific and clinical researchers. Read More

    Mechanisms of angiogenesis in microbe-regulated inflammatory and neoplastic conditions.
    Angiogenesis 2018 Feb 6;21(1):1-14. Epub 2017 Nov 6.
    Department of Biomedical Sciences, School of Pharmacy, Texas Tech University Health Sciences Center, Amarillo, TX, USA.
    Commensal microbiota inhabit all the mucosal surfaces of the human body. It plays significant roles during homeostatic conditions, and perturbations in numbers and/or products are associated with several pathological disorders. Angiogenesis, the process of new vessel formation, promotes embryonic development and critically modulates several biological processes during adulthood. Read More

    N-tert-butyloxycarbonyl-Phe-Leu-Phe-Leu-Phe (BOC2) inhibits the angiogenic activity of heparin-binding growth factors.
    Angiogenesis 2018 Feb 13;21(1):47-59. Epub 2017 Oct 13.
    Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
    The peptides N-tert-butyloxycarbonyl-Phe-Leu-Phe-Leu-Phe (BOC2) and BOC-Met-Leu-Phe (BOC1) are widely used antagonists of formyl peptide receptors (FPRs), BOC2 acting as an FPR1/FPR2 antagonist whereas BOC1 inhibits FPR1 only. Extensive investigations have been performed by using these FPR antagonists as a tool to assess the role of FPRs in physiological and pathological conditions. Based on previous observations from our laboratory, we assessed the possibility that BOC2 may exert also a direct inhibitory effect on the angiogenic activity of vascular endothelial growth factor-A (VEGF-A). Read More

    Notch signaling controls sprouting angiogenesis of endometriotic lesions.
    Angiogenesis 2018 Feb 9;21(1):37-46. Epub 2017 Oct 9.
    Institute for Clinical and Experimental Surgery, Saarland University, 66421, Homburg/Saar, Germany.
    Angiogenesis is essential for the engraftment and growth of endometriotic lesions. In this study, we analyzed whether this process is regulated by Notch signaling. Endometriotic lesions were induced by endometrial tissue transplantation into dorsal skinfold chambers of C57BL/6 mice, which were treated with the γ-secretase inhibitor DAPT or vehicle. Read More

    Antiangiogenesis and medical therapy failure in intracranial atherosclerosis.
    Angiogenesis 2018 Feb 9;21(1):23-35. Epub 2017 Oct 9.
    Department of Neurology, UCLA School of Medicine, Los Angeles, CA, USA.
    Intracranial atherosclerotic disease (ICAD) is one of the most common causes of stroke worldwide and the one with the worst prognosis. In this study, we assessed the hypothesis that the balance of circulating pro- and antiangiogenic factors plays a role in the evolution of the disease and can be used as a potential marker for the disease course and a target for treatment. Seventy-four patients with severe ICAD were enrolled in this prospective observational study, medically optimized, and followed for 6 months. Read More

    Pre-culture in endothelial growth medium enhances the angiogenic properties of adipose-derived stem/stromal cells.
    Angiogenesis 2018 Feb 7;21(1):15-22. Epub 2017 Oct 7.
    Department of Clinical Medicine, Ribeirão Preto Medical School, University of São Paulo, 3900 Bandeirantes Avenue, Ribeirão Preto, São Paulo, 14048-900, Brazil.
    Considerable progress has been made on the development of adipose-derived stem/stromal cells (ASCs) as pro-angiogenic therapeutic tools. However, variable clinical results highlight the need for devising strategies to enhance their therapeutic efficacy. Since ASCs proliferate and stabilize newly formed vessels during the angiogenic phase of adipose tissue formation, we hypothesized that mimicking an angiogenic milieu during culture of ASCs would enhance their capacity to support endothelial cell survival and angiogenesis. Read More

    Bone marrow sinusoidal endothelium: damage and potential regeneration following cancer radiotherapy or chemotherapy.
    Angiogenesis 2017 Nov 27;20(4):427-442. Epub 2017 Sep 27.
    Sansom Institute for Health Research, School of Pharmacy and Medical Sciences, University of South Australia, GPO Box 2471, Adelaide, SA, 5001, Australia.
    It is very well known that bone marrow (BM) microvasculature may possess a crucial role in the maintenance of homeostasis of BM due to mutual interactions between BM microvascular system and other physiological functions including haematopoiesis and osteogenesis. Chemotherapy and radiotherapy are known as main approaches for cancer treatment and also are known as the main cause of damage to the BM microvascular system. However, despite the importance of BM microvasculature in orchestrating various biological functions, less attention has been drawn to address the underlying mechanisms for the damage and to explore cellular and molecular mechanisms by which the recovery/regeneration of chemotherapy- and/or radiotherapy-induced BM microvascular system damage can occur. Read More

    A genomic screen for angiosuppressor genes in the tumor endothelium identifies a multifaceted angiostatic role for bromodomain containing 7 (BRD7).
    Angiogenesis 2017 Nov 26;20(4):641-654. Epub 2017 Sep 26.
    Angiogenesis Laboratory, Department of Medical Oncology, Cancer Center Amsterdam, VU University Medical Center, De Boelelaan 1117, 1081 HV, Amsterdam, The Netherlands.
    Tumor angiogenesis is characterized by deregulated gene expression in endothelial cells (EC). While studies until now have mainly focused on overexpressed genes in tumor endothelium, we here describe the identification of transcripts that are repressed in tumor endothelium and thus have potential suppressive effects on angiogenesis. We identified nineteen putative angiosuppressor genes, one of them being bromodomain containing 7 (BRD7), a gene that has been assigned tumor suppressor properties. Read More

    3D endothelial cell spheroid/human vitreous humor assay for the characterization of anti-angiogenic inhibitors for the treatment of proliferative diabetic retinopathy.
    Angiogenesis 2017 Nov 13;20(4):629-640. Epub 2017 Sep 13.
    Department of Molecular and Translational Medicine, University of Brescia, viale Europa 11, 25123, Brescia, Italy.
    Proliferative diabetic retinopathy (PDR) represents a main cause of acquired blindness. Despite the recognition of the key role exerted by vascular endothelial growth factor (VEGF) in the pathogenesis of PDR, limitations to anti-VEGF therapies do exist. Thus, rapid and cost-effective angiogenesis assays are crucial for the screening of anti-angiogenic drug candidates for PDR therapy. Read More

    Tumor vessel disintegration by maximum tolerable PFKFB3 blockade.
    Angiogenesis 2017 Nov 5;20(4):599-613. Epub 2017 Sep 5.
    Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, KU Leuven, 3000, Leuven, Belgium.
    Blockade of the glycolytic activator PFKFB3 in cancer cells (using a maximum tolerable dose of 70 mg/kg of the PFKFB3 blocker 3PO) inhibits tumor growth in preclinical models and is currently being tested as a novel anticancer treatment in phase I clinical trials. However, a detailed preclinical analysis of the effects of such maximum tolerable dose of a PFKFB3 blocker on the tumor vasculature is lacking, even though tumor endothelial cells are hyper-glycolytic. We report here that a high dose of 3PO (70 mg/kg), which inhibits cancer cell proliferation and reduces primary tumor growth, causes tumor vessel disintegration, suppresses endothelial cell growth for protracted periods, (model-dependently) aggravates tumor hypoxia, and compromises vascular barrier integrity, thereby rendering tumor vessels more leaky and facilitating cancer cell intravasation and dissemination. Read More

    Endothelial progenitor cells in multiple myeloma neovascularization: a brick to the wall.
    Angiogenesis 2017 Nov 24;20(4):443-462. Epub 2017 Aug 24.
    Research Institute for Medicines (iMed.ULisboa), Faculty of Pharmacy, Universidade de Lisboa, Av. Prof. Gama Pinto, 1649-003, Lisbon, Portugal.
    Multiple myeloma (MM) is characterized by the clonal expansion of plasma cells in the bone marrow that leads to events such as bone destruction, anaemia and renal failure. Despite the several therapeutic options available, there is still no effective cure, and the standard survival is up to 4 years. The evolution from the asymptomatic stage of monoclonal gammopathy of undetermined significance to MM and the progression of the disease itself are related to cellular and molecular alterations in the bone marrow microenvironment, including the development of the vasculature. Read More

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