Relevant bibliographies by topics / Neovascularization Regulation

Academic literature on the topic 'Neovascularization Regulation'

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Published: 10 December 2022
Last updated: 29 January 2023

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Journal articles on the topic "Neovascularization Regulation"

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Murakami, Masahiro, and Michael Simons. "Fibroblast growth factor regulation of neovascularization." Current Opinion in Hematology 15, no. 3 (May 2008): 215–20. http://dx.doi.org/10.1097/moh.0b013e3282f97d98.

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Wary, Kishore K., Erin E. Kohler, and Ishita Chatterjee. "Focal adhesion kinase regulation of neovascularization." Microvascular Research 83, no. 1 (January 2012): 64–70. http://dx.doi.org/10.1016/j.mvr.2011.05.002.

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Terao, Ryo, and Hiroki Kaneko. "Lipid Signaling in Ocular Neovascularization." International Journal of Molecular Sciences 21, no. 13 (July 4, 2020): 4758. http://dx.doi.org/10.3390/ijms21134758.

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Vasculogenesis and angiogenesis play a crucial role in embryonic development. Pathological neovascularization in ocular tissues can lead to vision-threatening vascular diseases, including proliferative diabetic retinopathy, retinal vein occlusion, retinopathy of prematurity, choroidal neovascularization, and corneal neovascularization. Neovascularization involves various cellular processes and signaling pathways and is regulated by angiogenic factors such as vascular endothelial growth factor (VEGF) and hypoxia-inducible factor (HIF). Modulating these circuits may represent a promising strategy to treat ocular neovascular diseases. Lipid mediators derived from membrane lipids are abundantly present in most tissues and exert a wide range of biological functions by regulating various signaling pathways. In particular, glycerophospholipids, sphingolipids, and polyunsaturated fatty acids exert potent pro-angiogenic or anti-angiogenic effects, according to the findings of numerous preclinical and clinical studies. In this review, we summarize the current knowledge regarding the regulation of ocular neovascularization by lipid mediators and their metabolites. A better understanding of the effects of lipid signaling in neovascularization may provide novel therapeutic strategies to treat ocular neovascular diseases and other human disorders.
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Leonhardt, Franziska, Sebastian Grundmann, Martin Behe, Franziska Bluhm, Rebecca A. Dumont, Friederike Braun, Melpomeni Fani, et al. "Inflammatory neovascularization during graft-versus-host disease is regulated by αv integrin and miR-100." Blood 121, no. 17 (April 25, 2013): 3307–18. http://dx.doi.org/10.1182/blood-2012-07-442665.

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Key Points Our data from the mouse model and patients indicate that inflammatory neovascularization during GvHD is targetable via αv integrin. We identify a negative regulation of GvHD-related neovascularization by miR-100.
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Xiang, Guosheng, Michael D. Schuster, Tetsunori Seki, Alfred A. Kocher, Shawdee Eshghi, Andrew Boyle, and Silviu Itescu. "Down-regulation of Plasminogen Activator Inhibitor 1 Expression Promotes Myocardial Neovascularization by Bone Marrow Progenitors." Journal of Experimental Medicine 200, no. 12 (December 13, 2004): 1657–66. http://dx.doi.org/10.1084/jem.20040221.

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Human adult bone marrow–derived endothelial progenitors, or angioblasts, induce neovascularization of infarcted myocardium via mechanisms involving both cell surface urokinase-type plasminogen activator, and interactions between β integrins and tissue vitronectin. Because each of these processes is regulated by plasminogen activator inhibitor (PAI)-1, we selectively down-regulated PAI-1 mRNA in the adult heart to examine the effects on postinfarct neovascularization and myocardial function. Sequence-specific catalytic DNA enzymes inhibited rat PAI-1 mRNA and protein expression in peri-infarct endothelium within 48 h of administration, and maintained down-regulation for at least 2 wk. PAI-1 inhibition enhanced vitronectin-dependent transendothelial migration of human bone marrow–derived CD34+ cells, and resulted in a striking augmentation of angioblast-dependent neovascularization. Development of large, thin-walled vessels at the peri-infarct region was accompanied by induction of proliferation and regeneration of endogenous cardiomyocytes and functional cardiac recovery. These results identify a causal relationship between elevated PAI-1 levels and poor outcome in patients with myocardial infarction through mechanisms that directly inhibit bone marrow–dependent neovascularization. Strategies that reduce myocardial PAI-1 expression appear capable of enhancing cardiac neovascularization, regeneration, and functional recovery after ischemic insult.
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Ishida, Susumu, Tomohiko Usui, Kenji Yamashiro, Yuichi Kaji, Shiro Amano, Yuichiro Ogura, Tetsuo Hida, et al. "VEGF164-mediated Inflammation Is Required for Pathological, but Not Physiological, Ischemia-induced Retinal Neovascularization." Journal of Experimental Medicine 198, no. 3 (August 4, 2003): 483–89. http://dx.doi.org/10.1084/jem.20022027.

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Hypoxia-induced VEGF governs both physiological retinal vascular development and pathological retinal neovascularization. In the current paper, the mechanisms of physiological and pathological neovascularization are compared and contrasted. During pathological neovascularization, both the absolute and relative expression levels for VEGF164 increased to a greater degree than during physiological neovascularization. Furthermore, extensive leukocyte adhesion was observed at the leading edge of pathological, but not physiological, neovascularization. When a VEGF164-specific neutralizing aptamer was administered, it potently suppressed the leukocyte adhesion and pathological neovascularization, whereas it had little or no effect on physiological neovascularization. In parallel experiments, genetically altered VEGF164-deficient (VEGF120/188) mice exhibited no difference in physiological neovascularization when compared with wild-type (VEGF+/+) controls. In contrast, administration of a VEGFR-1/Fc fusion protein, which blocks all VEGF isoforms, led to significant suppression of both pathological and physiological neovascularization. In addition, the targeted inactivation of monocyte lineage cells with clodronate-liposomes led to the suppression of pathological neovascularization. Conversely, the blockade of T lymphocyte–mediated immune responses with an anti-CD2 antibody exacerbated pathological neovascularization. These data highlight important molecular and cellular differences between physiological and pathological retinal neovascularization. During pathological neovascularization, VEGF164 selectively induces inflammation and cellular immunity. These processes provide positive and negative angiogenic regulation, respectively. Together, new therapeutic approaches for selectively targeting pathological, but not physiological, retinal neovascularization are outlined.
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Burtenshaw, Denise, and Paul A. Cahill. "Natriuretic Peptides and the Regulation of Retinal Neovascularization." Arteriosclerosis, Thrombosis, and Vascular Biology 40, no. 1 (January 2020): 7–10. http://dx.doi.org/10.1161/atvbaha.119.313566.

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Battinelli, Elisabeth M. "Platelet and Megakaryocytic Regulation of Tumor Progression." Blood 130, Suppl_1 (December 7, 2017): SCI—26—SCI—26. http://dx.doi.org/10.1182/blood.v130.suppl_1.sci-26.sci-26.

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Traditionally viewed as the bandaids of the blood, the contribution of platelets to the progression of malignancy is emerging as a compelling focus for therapeutic intervention. Complex interactions between tumor cells, and circulating platelets play an important role in tumor growth and dissemination, and a growing body of data supports a role for platelet activation and release of chemokines in metastases and neovascularization. Supporting this concept is the evidence that elevated platelet counts (thrombocytosis) at time of diagnosis with malignancy is a harbinger of an aggressive cancer with a poor prognosis. One very interesting and provocative connection between cancer and platelets is the increasing evidence that tumor cells hijack platelets to promote a more pro-malignant phenotype to drive disease progression. Our laboratories have been instrumental in establishing the pro-malignant role of platelets in metastasis and neovascularization. We have demonstrated that tumor cells can instruct platelets to release key cytokines that promote angiogenesis and metastasis of tumor cells. Perhaps the most compelling clinical evidence of the link between platelets and malignancy is the finding that anti-platelet agents can have a profound impact on malignancy. We have demonstrated previously, anti-platelet agents such as aspirin and anticoagulants suppress release of key neovascularization factors from platelets and suppress the neovascularization potential. Aspirin also suppresses the invasive properties of platelets in mouse metastasis models as well as in vitro metastasis assays. Similarly, we have also demonstrated that tamoxifen, a selective estrogen receptor modulator often used to treat breast cancer, can also diminish the ability of platelets to support malignancy by diminishing the platelet's role in promoting neovascularization as well as metastasis. Although much is understood regarding how tumors communicate with platelets less is understood about how platelets manipulate tumor cells. Our laboratory has elucidated the role of key chemokines released from platelets in response to tumor cells and how these factors promote tumor growth and metastasis. We have recently discovered that tumor cells can instruct platelets to release CCL5, a known driver of tumor cell invasion and metastasis, and have expanded the role of CCL5 not only as a regulator of metastasis but also as a central controller of platelet production. Despite this progress many questions still remain regarding the interaction between tumor cells and platelets. We are particularly interested in how tumor cells instruct megakaryocytes to increase platelet production. In addition malignancy may also reprogram megakaryocytes thereby manipulating the platelet phenotype to support tumor growth and metastasis. Because most cancer therapies focus on the tumor itself, the idea of targeting platelets in the tumor microenvironment to arrest tumor growth and metastatic spread represents a novel therapeutic strategy. Disclosures No relevant conflicts of interest to declare.
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Walter, Dirk H., and Stefanie Dimmeler. "Endothelial Progenitor Cells: Regulation and Contribution to Adult Neovascularization." Herz 27, no. 7 (November 1, 2002): 579–88. http://dx.doi.org/10.1007/s00059-002-2427-y.

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Li, Fengkai, Jiahui Xu, and Suling Liu. "Cancer Stem Cells and Neovascularization." Cells 10, no. 5 (April 30, 2021): 1070. http://dx.doi.org/10.3390/cells10051070.

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Cancer stem cells (CSCs) refer to a subpopulation of cancer cells responsible for tumorigenesis, metastasis, and drug resistance. Increasing evidence suggests that CSC-associated tumor neovascularization partially contributes to the failure of cancer treatment. In this review, we discuss the roles of CSCs on tumor-associated angiogenesis via trans-differentiation or forming the capillary-like vasculogenic mimicry, as well as the roles of CSCs on facilitating endothelial cell-involved angiogenesis to support tumor progression and metastasis. Furthermore, we discuss the underlying regulation mechanisms, including the intrinsic signals of CSCs and the extrinsic signals such as cytokines from the tumor microenvironment. Further research is required to identify and verify some novel targets to develop efficient therapeutic approaches for more efficient cancer treatment through interfering CSC-mediated neovascularization.
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Dissertations / Theses on the topic "Neovascularization Regulation"

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Singhal, Mahak [Verfasser], and Ana [Akademischer Betreuer] Martin-Villalba. "Angio-regulation of liver neovascularization and lung metastatic progression / Mahak Singhal ; Betreuer: Ana Martin-Villalba." Heidelberg : Universitätsbibliothek Heidelberg, 2020. http://d-nb.info/1236403088/34.

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Zheng, Feihui, and 郑斐晖. "Up-regulation of alpha-enolase (ENO1) by HIF-1α in retinal pigment epithelial cells after hypoxic challenge is not involved in the regulation of VEGF secretion." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/208585.

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Choroidal neovascularization (CNV) is a leading threat to severe vision loss, particularly in patients with age-related macular degeneration (AMD). In CNV, newly formed blood vessels sprout from the choroid to the sub-retinal space, where leakage and bleeding of the abnormal vessels lead to photoreceptor death and subsequent vision loss. It is believed that CNV is mediated by growth factors (e.g. vascular endothelial growth factor {VEGF}) produced by the retinal pigment epithelium (RPE) under pathological states (e.g. hypoxia). Current treatments for CNV aiming at countering VEGF only help decrease leakage and inhibit formation of CNV, but none of them is curative and the recurrence rate remains high. In order to find other more powerful potential therapeutic targets, the regulations of VEGF signaling in the pathophysiology of CNV is the focus of numerous translational investigations. Previously, Hypoxia-inducible factor-1 (HIF-1), a crucial transcriptional factor in response to hypoxia, is identified as the master transcriptional factor controlling VEGF expression in the RPE promoting CNV. Alpha-enolase (ENO1), a key glycolytic enzyme, is known to be over expressed in several types of carcinomas also under the regulation of HIF-1. ENO1 has been reported to be closely associated with cancer progression, angiogenesis, and venous invasion. The molecular events of ENO1 in the pathogenesis of promoting angiogenesis are of interest but still barely understood. Recently, the association of ENO1 antibodies with retina has been seen in patients with AMD. We hypothesize that ENO1 expression in the RPE may play a role in the development of CNV, participating in the regulation of VEGF. Hypoxia is an important pathological condition in the formation of CNV. Here, we first determined ENO1 expression and cell death in a human RPE cell line, ARPE-19, under cobalt (II) chloride (CoCl2)-induced hypoxia or anoxia (95% N2, 5% CO2). To further investigate the regulation of ENO1 in CNV, HIF-1α-diminished RPE cells were generated using small interfering RNA (siRNA) and the change of ENO1 expression in response to hypoxic injury was determined. Upon 24 hr of treatment with CoCl2-induced hypoxia or anoxia, the expression of ENO1 and VEGF increased significantly along with HIF-1α in ARPE-19 cells, both of which could in turn be significantly down-regulated by HIF-1α siRNA. Interestingly, cell death remained low in ARPE-19 cells, even after 24 hr of CoCl2-induced hypoxia or anoxia. To further study the role of ENO1 in CNV, we started by investigating the relationship between ENO1 and VEGF. SiRNA was used to knock down the expression of ENO1 in ARPE-19 cells. Upon transfection with the siRNA, ENO1 expression was successfully down-regulated when treated with CoCl2-induced hypoxia. However, VEGF secretions from the ENO1-diminished ARPE-19 cells under CoCl2-induced hypoxia remained unchanged. Double knockdown of ENO1 together with HIF-1α by siRNA also did not help to further suppress VEGF secretion in the hypoxic ARPE-19 cells. Hence, ENO1 was demonstrated to be activated and up-regulated by HIF-1 in RPE cells responding to hypoxia, suggesting a potential role of ENO1 in favoring the formation of CNV, but not through influencing VEGF secretion.
published_or_final_version
Ophthalmology
Master
Master of Philosophy
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Angulo, Urarte Ana. "Regulation of actomyosin contractility by p110α P13-kinase in sprouting angiogenesis." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/401498.

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Class IA PI3K (PI3K) functions have been widely investigated over the last two decades. PI3K signalling is located at the crossroads of many cell surface receptors sending signals to coordinate multiple cellular functions such as cell growth, survival, motility, and metabolism. Fine-tune regulation of PI3K signalling in cells is needed to ensure the functionality of tissues and organs. However, it is still not clear how or even which PI3K isoforms are concerted into precise morphogenic events. On the other hand, PI3K activity plays central roles in several cellular processes critical for cancer progression. Hence, PI3K pathway inhibition is considered an important target for therapeutic intervention in cancer, and progress in the clinical area is being monitored by many clinical trials with PI3K inhibitors. We were interested in investigating the role of PI3K activity in endothelial cells during the process of angiogenesis. Although ECs express all class I PI3K isoforms, only inactivation of the catalytic subunit p110α in endothelial cells (not p110β or p110δ inactivation) leads to vascular defects in the embryo (Graupera et al. 2008). This indicates that p110α activity in ECs is required in a cell- autonomous manner to ensure proper vascular development and remodelling during the embryogenesis. However, progress in the understanding of how p110α-PI3K signalling regulates the different steps of vascular morphogenesis has been hampered by embryonic lethality that both the constitutive and endothelial specific p110α mutant mice exhibit. By using a tamoxifen-inducible endothelial Cre line in mouse and genetic and pharmacological approaches in zebrafish embryos, we have found that p110α signalling is required to maintain vessel stability. The lack of p110α activity leads to endothelial tubular structures composed of single cells that show an elongated shape with multiple protrusions and no lumen. These ECs fail in the elongation of the inter-endothelial contacts during the sprout outgrowth. Furthermore, I found that p110α is involve in the initial steps of fusion and is necessary for proper establishment of a new connection. Finally, I identifyed that p110α negatively controls actomyosin contractility independently of Rho/ROCK signalling pathway and that this control could be exerted through the regulation of MLC phosphatase activity by the impact on mRIP and/or MYPT proteins.
La señalización PI3K de clase IA se requiere de una manera autónoma en células endoteliales para el correcto crecimiento de los vasos sanguíneos. Aunque las células endoteliales expresan todas las isoformas de la clase IA de PI3Ks, sólo la subunidad catalítica p110α es necesaria para la angiogenesis fisiológica. Sin embargo, poco se sabe sobre el papel de p110α -PI3K en las diferentes etapas de la morfogénesis vascular. Mediante la generación de una línea inducible Cre endotelial de ratón y la inactivación genética y farmacológica de la proteína en embriones de pez cebra, hemos encontrado que la señalización a través de la proteína p110α es necesaria para mantener la estabilidad del los vasos sanguíneos. La falta de la actividad de la proteína p110α da lugar a la formación de una vasculatura aberrante formada por estructuras endoteliales muy delgadas compuestas por células individuales que emiten múltiples protrusiones y carecen de lumen. Durante la elongación del nuevo brote vascular las células endoteliales no puede elongar la superficie de adhesión entre células endoteliales y por tanto no pueden sufrir reordenamientos necesarios para el crecimiento del nuevo vaso. También hemos visto que la proteína p110α está implicada en la estabilización de los nuevos contactos durante el proceso de anastomosis vascular y su inactivación da lugar a inestabilidad vascular y la aparición de desconexiones en entre vasos. La falta de la proteína p110α se asocia con un aumento en la formación de los cables de actina cortical e hiperfosforilacion de la cadena ligera de la miosina. Por tanto, identificamos que la ruta de señalización p110α-PI3K controla negativamente la contractilidad de las fibras de actomiosina de forma independiente a la via de señalización Rho-ROCK y que este control podría ser ejercido a través de la regulación de la actividad de la fosfatasa MLC a través de las proteínas mRIP y/o MYPT1.
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Calderone, Vittorio. "Regulation of angiogenesis by CPEB-mediated translational control." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/120702.

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Hepatic cirrhosis is a largely diffused pathology caused by alcohol abuse and hepatitis C in developed countries, whereas hepatitis B is the cause in most parts of Asia and sub-Saharan Africa. It's characterized by development of regenerative nodules delimited by fibrous septa. Regenerative nodules are composed by proliferating hepatocytes, entrapped by deposition of extracellular matrix, and have been shown to be involved in growth factor production, in particular VEGF, which is responsible of angiogenic induction that culminates with formation of a dense network of blood vessels into fibrous septa. The newly formed blood vessels of fibrous septa connect the vessels of the portal region with terminal hepatic veins, determining an alternative route of the blood flow that, in this way, is redirected into the systemic circulation bypassing the liver. At pre-hepatic level, the cirrhosisrelated portal hypertension induces development of new blood vessels that shunt the portal blood into the systemic circulation. As consequence of both intrahepatic and pre-hepatic angiogenesis, the liver cannot metabolize several blood components such as drugs, nutrients, toxins, and bacteria, with obvious deleterious effects. Despite angiogenesis is one of the main complications of liver cirrhosis and VEGF has a pivotal role in the control of blood vessels formation, the molecular mechanisms that govern VEGF expression during angiogenesis and hepatic cirrhosis are poorly understood. In order to address whether CPEB family of proteins may have a function in the regulation of angiogenesis in liver diseases, we analysed the expression of CPEBl and CPEB4 in liver of patients affected by hepatic cirrhosis. The expression of CPEBl and CPEB4 was increased in regenerative nodules, compared with basal levels of expression detected in healthy hepatic parenchyma. Interestingly, also VEGF expression was higher in regenerative nodules. The numerous fibrous septa that characterized cirrhotic livers resulted highly vascularized, and the endothelium of newly formed blood vessels expressed high levels of CPEB1, CPEB4 and VEGF. The description of CPEB1, CPEB4 and VEGF expression in healthy and cirrhotic conditions represented a first cue of CPEB-mediated translational regulation of VEGF mRNA during angiogenesis. To prove the accuracy of this hypothesis we implemented two animal models that allowed the study of intrahepatic and prehepatic angiogenesis correlated with liver cirrhosis. CBDL experiments performed in rats enabled to recapitulate the histopathological conditions observed in human hepatic cirrhosis. Cirrhotic rat livers showed deep histological perturbations, with high proliferation of blood vessels and biliary ducts. Compared with control healthy samples, the expression of CPEB1, CPEB4 and VEGF in pathological liver was strongly increased. These proteins localized at level of both, blood vessels and biliary ducts. Partial portal vein ligation (PPVL) experiments performed in rats enabled to show an important correlation between CPEBl and CPEB4 expression with VEGF synthesis and consequent high vascularization of mesentery. In angiogenic condition, both pre-existing and newly formed blood vessels expressed CPEB1, CPEB4 and VEGF at level of endothelium, smooth muscle and adventitia, tissues that playa pivotal role in the development of the vascular net. To better define the mechanistic relevance of these correlations, we characterized the endothelial cell line HSV. In this in vitro model we modulated the levels of CPEBl and CPEB4, and showed a direct involvement of this two proteins in the translational regulation of VEGF mRNA. Taking advance of the ability of HSV cells to form blood vessel like structure in an in vitro angiogenesis assay, we were able to show that CPEBl and CPEB4 are required for VEGF synthesis and secretion, which in turn are essential to create the correct microenvironment necessary to activate the cells and induce the formation of a dense network of vascular structures on Matrigel. Our results suggest that CPEBl drives the nuclear cleavage of VEGF 3'UTR while CPEB4 is responsible of its cytoplasmic polyadenylation.
"Regulación de la angiogénesis a través del control traduccional mediato par las proteínas CPEB " En muchas enfermedades hepáticas cr6nicas, la angiogénesis es una importante característica patológica y juega un papel crucial en la progresión de la fibrogénesis hepática a cirrosis, y en la aparición y agravamiento de la hipertensión portal, la cual determina las principales complicaciones de la enfermedad. A pesar de que es evidente que VEGF es el principal efector de la angiogénesis patológica, los mecanismos moleculares que gobiernan la activación post-transcripcional de su síntesis durante la cirrosis hepática son en gran parte desconocidos. En este trabajo se muestra que la síntesis de VEGF está regulada a través de funciones secuenciales y no redundantes de dos miembros de la familia de las proteínas CPEB:. CPEB1 y CPEB4. Por 10 tanto, CPEB1 promueve el procesamiento alternativo de ambos los pre-ARNm de CPEB4 y VEGF, acortando las 3'UTRs y excluyendo elementos de inhibición de la traducción de los transcritos maduros. Como resultado de este procesamiento alternativo, CPEB4 se sobreexpresa, y polyadenyla el ARNm de VEGF, aumentando aún más su traducción. Entonces, se requieren tanto CPEB1 como CPEB4 para la síntesis de VEGF y la consecuente angiogénesis. Por tanto, todas las proteínas se sobreexpresan de forma secuencial en pacientes y en modelos animales de cirrosis hepática e hipertensión portal, y ambos ratones knock-out para CPEB1 y CPEB4 no lograron activar la angiogénesis tras la inducción de hipertensión portal. A través del análisis de la angiogénesis en ensayos in vitro, las muestras de humanos y modelos animales, nuestros resultados ponen de relieve el papel crucial de CPEBs en la neovascularización patol6gica, en el marco de la hipertensión portal y cirrosis, e identifican CPEBs como potenciales nuevas dianas moleculares para el tratamiento de la enfermedad hepática cr6nica y otras enfermedades dependientes de la neovascularización, como el cáncer.
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Jang, Wai-chi. "Responses of retinal pigment epithelial cells to anoxic/hypoxic stress after hypoxia-inducible factor-1-alpha down-regulation." Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43571980.

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Azzarello, Joseph Thaddeus. "Angiogenesis regulation and control at the ligand/receptor level and beyond /." Oklahoma City : [s.n.], 2009.

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Jang, Wai-chi, and 張慧芝. "Responses of retinal pigment epithelial cells to anoxic/hypoxic stressafter hypoxia-inducible factor-1-alpha down-regulation." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43571980.

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Monelli, Erika. "Deciphering the role of endothelial cells in the regulation of physiological and pathological white adipose tissue remodelling." Doctoral thesis, Universitat de Barcelona, 2017. http://hdl.handle.net/10803/572073.

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In response to nutritional variation, white adipose tissue (WAT) undergoes a physiological remodelling that involves qualitative and quantitative changes in resident cells and is coordinated with angiogenesis. In a condition of chronic over nutrition WAT expansion is associated to insufficient vascularisation which in turn leads to local hypoxia, inflammation and adipocytes death (hallmark of obesity). Currently, enhanced WAT angiogenesis is believed to be a promising intervention to ameliorate obesity associated metabolic dysfunctions. However, we still lack understanding of the cell intrinsic function of endothelial cells in WAT remodelling. Here we take advantage of our mouse model of PTEN (a dual lipid/protein phosphatase that counterbalance the activity of PI3K) deletion in ECs to promote vessel growth, in a cell autonomous manner. To this end, we crossed Ptenflox/flox mice with PdgfbiCreERT2 transgenic mice that express a tamoxifen-inducible Cre recombinase in ECs; 4-hydroxytamoxifen was administered in vivo at postnatal day 1 (P1) and P2 to activate Cre expression. Increased ECs proliferation, induced by PTEN loss, promotes vascular hyperplasia exclusively in WAT and leads to a progressive loss of WAT mass. PTEN null ECs undergo a metabolic switch towards an oxidative metabolism; in vivo inhibition of - oxidation is sufficient to revert both vascular hyperplasia and loss of WAT mass. Enhanced adipose vascularisation prevents from high fat diet induced WAT hypertrophy, limits body weight gain and improves glucose tolerance. Taken together our results suggest that, under obesogenic stimuli, more functional ECs prevent unhealthy WAT expansion and consequently the onset of obesity related comorbidity.
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Wang, Ying. "The role of the hypoxia-inducible factor pathway in bone development and repair." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/wang.pdf.

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Horckmans, Michael. "Rôle des nucléotides extracellulaires dans la régulation de l'angiogénèse, l'inflammation et le développement cardiaque." Doctoral thesis, Universite Libre de Bruxelles, 2009. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210204.

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Notre travail a permis tout d’abord d’investiguer les effets des nucléotides extracellulaires sur les cellules

dendritiques (DCs) qui sont des cellules présentatrices d’antigènes capables d’initier et de réguler la

réponse immunitaire. Afin d’avoir une vue globale de l’action des nucléotides extracellulaires sur les DCs,

un profil d’expression génique de l’ATPgS – dérivé stable de l’ATP - a été réalisé par microarray dans les

cellules dendritiques dérivées de monocytes (MoDCs).

Notre groupe a préalablement montré que malgré que l’ATP est considéré comme un signal de danger, il

confère des propriétés immunosuppressives aux DCs (Marteau et al, 2005). Nous nous sommes focalisés

sur des régulations géniques pouvant être mises en relation avec un action anti-inflammatoire de l’ATP.

Nous avons ainsi démontré que l’ATP était capable d’inhiber la sécrétion des chimiokines MCP-1 et MIP-

1a initiée par l’action du LPS, ce qui a pour conséquence de diminuer la capacité des DCs à recruter des

monocytes ou d’autres DCs. Ce travail a fait l’objet d’une publication en tant que premier auteur

(Horckmans et al, 2005).

Un grand nombre d’autres gènes régulés liés à la réponse immune et à l’inflammation a été identifiée

dans le profil microarray de l’ATPgS. Nous avions notamment pu identifier une augmentation de la

sécrétion de VEGF-A en réponse à l’ATP, amplifiée en présence de LPS. Cette régulation est extrêmement

intéressante au vu de l’action immunosuppressive du VEGF sur les DCs. Par ailleurs, cette régulation

pourrait constituer un lien entre les DCs et l’angiogénese. Ce travail a fait l’objet d’une publication en tant

que premier co-auteur dans la revue Journal of Immunology (Bles et al, 2007).

En conclusion, nos données nous ont ainsi permis de montrer que les nucléotides adényliques peuvent

avoir par leur action sur les cellules dendritiques une action anti-inflammatoire voire pro-angiogénique,

en inhibant le recrutement leucocytaire et une action immunosuppressive en stimulant la sécrétion de

VEGF.


Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished

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Books on the topic "Neovascularization Regulation"

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Biophysical regulation of vascular differentiation and assembly. New York: Springer, 2011.

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J, Tomanek Robert, ed. Assembly of the vasculature and its regulation. Boston: Birkhäuser, 2002.

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1911-, Foà Piero P., ed. Humoral factors in the regulation of tissue growth: Blood, blood vessels, skeletal system, and teeth. New York: Springer-Verlag, 1993.

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Harmey, Judith H. VEGF and cancer. Georgetown, Tex: Landes Bioscience/Eurekah.com, 2004.

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1948-, Goldberg I. D., and Rosen E. M, eds. Regulation of angiogenesis. Basel: Birkhäuser, 1997.

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Regulation Angiogenesis (EXS). Birkhauser, 1996.

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Tomanek, Robert J. Assembly of the Vasculature and Its Regulation. Springer, 2012.

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Gerecht, Sharon. Biophysical Regulation of Vascular Differentiation and Assembly. Springer, 2011.

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Gerecht, Sharon. Biophysical Regulation of Vascular Differentiation and Assembly. Springer New York, 2013.

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Gerecht, Sharon. Biophysical Regulation of Vascular Differentiation and Assembly. Springer, 2018.

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Book chapters on the topic "Neovascularization Regulation"

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Trane, Andy E., and Pascal N. Bernatchez. "Therapeutic Insight Into Reactive Oxygen Species Regulation of Neovascularization." In Systems Biology of Free Radicals and Antioxidants, 1537–54. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-30018-9_60.

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Frank, Robert N., and Laura B. Sotolongo. "Growth Factors and the Retina: Normal Vascularization and Pathologic Neovascularization." In Humoral Factors in the Regulation of Tissue Growth, 18–46. New York, NY: Springer New York, 1993. http://dx.doi.org/10.1007/978-1-4613-9272-9_2.

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Polverini, Peter J. "Inhibitors of Neovascularization: Critical Mediators in the Coordinate Regulation of Angiogenesis." In Angiogenesis, 29–37. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4757-9188-4_4.

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G. Singh, Pooja, Kanthesh M. Basalingappa, T. S. Gopenath, and B. V. Sushma. "Tumour Angiogenesis in Breast Cancer." In Tumor Angiogenesis [Working Title]. IntechOpen, 2022. http://dx.doi.org/10.5772/intechopen.102944.

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Since the last comprehensive assessment of antiangiogenic therapy was published in Breast Cancer Research 3 years ago, clinical trials in a variety of tumour types, including breast cancer, have underscored the key relevance of tumour neovascularization. Bevacizumab, a drug designed to target vascular endothelial cell growth factor, was utilised in many of these studies (VEGF). Clinical trials using antiangiogenic treatment in breast cancer have highlighted the critical role of tumour neovascularization. Personalised medicine will become increasingly important to generate maximum therapeutic benefit to the patient but also to realise the optimal economic advantage from the finite resources available, according to a report by the US Department of Health and Human Services (HHS) and the National Institute for Occupational and Environmental Health (NIH). This overview covers the history of breast tumour neovascularization in both in situ and invasive breast cancer, the processes by which it occurs, and the impact of the microenvironment, with a focus on hypoxia. The regulation of angiogenesis, as well as the antivascular drugs employed in antiangiogenic dosing schedules, both innovative and traditional, are discussed.
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Gunda, Venugopal, and Yakkanti A. "Regulation of Angiogenesis in Choroidal Neovascularization of Age Related Macular Degeneration by Endogenous Angioinhibitors." In Advances in Ophthalmology. InTech, 2012. http://dx.doi.org/10.5772/26807.

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Khan, Rujman, Xin Yee Ooi, Matthew Parvus, Laura Valdez, and Andrew Tsin. "Advanced Glycation End Products: Formation, Role in Diabetic Complications, and Potential in Clinical Applications." In The Eye and Foot in Diabetes. IntechOpen, 2020. http://dx.doi.org/10.5772/intechopen.89408.

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Hyperglycemic conditions and disruptions to glucose-regulating pathways lead to increased formation of highly reactive aldehydes, methylglyoxal and glyoxal, which react with certain arginine and lysine residues in proteins to form advanced glycation end products (AGEs). These AGEs damage the integrity of the retinal vasculature predominantly through two mechanisms: non-receptor-mediated damage, which pertains to the interaction with extracellular matrix and its functional properties, and receptor-mediated damage through AGE interactions with their receptors (RAGE) on pericytes and Muller cells. Damage occurring between AGE and RAGE potentially generates reactive oxygen species, inflammatory cytokines, and growth factors. Both mechanisms result in increased permeability of endothelial tight junctions, and this increased permeability can lead to leaking and eventually ischemia. Once this ischemia becomes significant, neovascularization can occur, the hallmark of proliferative diabetic retinopathy. Current pharmaceutical studies have shown the potential of AGE inhibitors, such as aminoguanidine, in decreasing AGE production, thus minimizing its effects in hyperglycemic conditions. Other pharmaceutical interventions, such as Tanshinone IIA, aim to protect cells from the impacts of AGEs. Future research will not only continue to understand the properties of AGEs and their effects on diabetes and diabetic complications like diabetic retinopathy but will also explore how they impact other diseases.
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Conference papers on the topic "Neovascularization Regulation"

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Deng, Weimin, Yi Lu, Xin Gu, Paulina Huang Liang, Zhi Yao, and Luyuan Li. "Abstract 468: Down-regulation of TNFSF15 (VEGI) in tumor vasculature under inflammatory conditions is a pre-requisite of tumor neovascularization." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-468.

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Hurley, Jennifer R., and Daria A. Narmoneva. "Endothelial-Fibroblast Interactions in Angiogenesis and Matrix Remodeling." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206534.

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Revascularization is critical for successful regeneration of ischemic cardiac tissue after injury. To achieve revascularization in engineered cardiac grafts, it is necessary to understand the interactions between major cardiac cell types. The importance of cardiomyocyte-endothelial interactions in angiogenesis is well documented [1]; however, less is known about interactions between endothelial and stromal cells, fibroblasts in particular. Studies indicate that during capillary assembly, fibroblasts (FBs) provide chemical signaling via growth factor expression and endothelial activation and proliferation [2]. In addition, fibroblasts deposit extracellular matrix (ECM) proteins [3] and also play a role in matrix remodeling. The objective of our study was to further investigate the role of endothelial-fibroblast interactions in angiogenesis with a focus on FB regulation of the extracellular mechanical environment. We and others have recently shown that self-assembling peptide nanoscaffold is a promising material for cardiac tissue regeneration, enhancing angiogenesis in vitro and promoting tissue neovascularization in vivo [1, 4–5]. An important advantage of this nanoscaffold is the ability to control its material properties, such as stiffness and rate of MMP degradation, through its sequence and/or concentration [6]. In this study, RAD16-II peptide nanoscaffold was used as a controlled system to test the hypothesis that fibroblasts regulate angiogenesis via modifying the extracellular mechanical environment through mechanisms including cell-mediated scaffold disruption and matrix remodeling.
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Buchanan, Cara F., Elizabeth Voigt, Christopher S. Szot, Joseph W. Freeman, Pavlos P. Vlachos, and Marissa Nichole Rylander. "Shear Stress Mediates Angiogenic Gene Expression in a Microfluidic Tumor Vascular Model." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80286.

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While research has shown that the fluid mechanics of the tumor vasculature reduce transport and uptake of therapeutics, the underlying role of these stresses in regulating tumor-endothelial cell signaling and neovascularization are not well understood. Understanding the reciprocal interaction between endothelial and tumor cells to mediate angiogenesis, and the effect of fluid shear on this process, may offer insight into the development of improved treatment modalities to control highly vascularized tumors. We have previously shown that breast cancer cells cultured under 2D, static conditions with endothelial cells significantly increase expression of pro-angiogenic factors vascular endothelial growth factor (VEGF) and angiopoietin 2 (ANG2) [1]. These preliminary results motivated the investigation of tumor-endothelial cross-talk under 3D, dynamic co-culture conditions.
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Buchanan, Cara F., Elizabeth Voigt, Christopher S. Szot, Joseph W. Freeman, Pavlos P. Vlachos, and M. Nichole Rylander. "Development of a 3D Microfluidic Culture Model to Study the Effect of Shear Stress on Tumor Angiogenesis." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53910.

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Current in vitro studies of tumor angiogenesis and metastasis are limited by the use of static 2D culture systems or 3D models that poorly reflect the pathological tumor microenvironment. While these systems have provided insight into tumor-inherent mechanisms of neovascularization, they are unable to couple local cellular response with specific biochemical and mechanical cues [1]. Interstitial flow plays an important role in regulating tumor growth; however, there are currently no in vitro cell culture models specifically designed to investigate the effect of fluid shear on tumorigenesis. By integrating tissue-engineering strategies with microfluidics and particle image velocimetry, we have developed a 3D in vitro cell culture model that allows the relationship between shear stress and tumor-endothelial cell cross-talk to be monitored. This research strategy will greatly improve our understanding of shear-stress mediated angiogenesis.
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Cho, Hongkwan, Abdul Sheikh, and Daria A. Narmoneva. "Non-Specific Endothelial Cell Interactions With the Substrate Result in Cell Activation and Angiogenesis In Vitro." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19094.

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Vascularization is critical for success of tissue engineering applications. Previous studies by us and others have shown that self-assembling peptide nanoscaffold RAD16-II promotes de novo capillary formation (angiogenesis) in vitro and neovascularization in vivo, and is a promising material for tissue engineering applications [1, 2]. However, the molecular mechanisms for cell interactions with this material are not known. Angiogenesis is mediated via interactions between integrins, which are expressed on the surface of activated endothelial cells (ECs), and extracellular matrix proteins. Among several integrins, αvβ3 is the most abundant and influential receptor regulating angiogenesis [3]. The αvβ3 integrin binds to its ligands via Arg-Gly-Asp (RGD) biding motif. However, there are no RGD motifs on RAD 16-II peptide. Instead, it contains three RAD motifs. Studies have shown that non-specific binding of αvβ3 with RAD can be retained through R and D sides [4]. The objective of this study, therefore, is to elucidate the underlying molecular mechanisms of RAD16-II nanoscaffold interactions with microvascular endothelial cells. We hypothesize that non-specific interactions between RAD16-II peptide nanoscaffold and αvβ3 integrin result in phosphorylations of β3 cytoplasmic domain, which then activate downstream angiogenic signaling pathways and promote angiogenesis.
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