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Academic literature on the topic 'VEGF165b'

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Published: 10 March 2023

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Journal articles on the topic "VEGF165b"

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Garcia-Foncillas, Jesus, Manuel Domine, Federico Rojo, Tatiana Hernandez, Sandra Zazo, Gloria Serrano, Cristina Chamizo, et al. "VEGF-A 165 family of isoforms as predictive biomarkers in patients with nonsquamous non-small cell lung cancer (NSCLC) treated with bevacizumab." Journal of Clinical Oncology 31, no. 15_suppl (May 20, 2013): e19109-e19109. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e19109.

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e19109 Background: Bevacizumab is a recombinant monoclonal humanized antibody to vascular endothelial growth factor (VEGF) that improves Time to Progression (TTP) in patients with advanced non-squamous NSCLC in combination with a doublet of platins, but currently no proven predictive markers exist. The VEGF-A 165 splice variant has been described as the most abundant and active isoform in cancer. Exon 8 splice modifications of VEGF 165 generates the VEGF-A 165a family of isoforms, which has a pro-angiogenic effect, and VEGF-A 165b family, with an anti-angiogenic activity. This study is aimed to explore the role of VEGF165a and VEGF165b expression in tumors as predictive biomarkers of efficacy in patients with NSCLC treated with platins plus bevacizumab. Methods: 22 patients were included (20 adenocarcinomas and 2 large cell carcinomas): 5 received carboplatin-taxol-bevacizumab, 14 carboplatin-taxotere-bevacizumab and 3 cisplatin-gemcitabine-bevacizumab. Total RNA was isolated by RNeasy FFPE procedure. VEGF165a and VEGF165b expression was analyzed by RT-qPCR using appropriate specific primers and probes. Individual VEGF165a and VEGF165b family of isoforms expression was calibrated to normal tissue and the ratio between both isoforms was calculated. Results: VEGF165a overexpression was detected in 14 (63.6%) cases and VEGF165b overexpression in 15 (68.2%). Individual overexpression for each family of isoforms was not predictive of benefit to bevacizumab therapy (p=0.933 and 0.166). However, the ratio between VEGF165a and VEGF165b was associated with TTP, correlating a predominant expression of pro-angiogenic VEGF165a with a significant benefit compared with cases with predominant VEGF165b expression (median TTP, 15 vs. 8 months respectively, p=0.005). The expression of both isoforms did not impact on OS (p=0.477). Conclusions: The overexpression of VEGF165a and low expression of VEGF165b family of isoforms correlated with benefit to anti-angiogenic therapy in NSCLC patients, supporting a potential use as predictive biomarkers for bevacizumab treatment in stage IV non-squamous NSCLC.
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Varet, Julia, Samantha K. Douglas, Laura Gilmartin, Andrew R. L. Medford, David O. Bates, Steven J. Harper, and Ann B. Millar. "VEGF in the lung: a role for novel isoforms." American Journal of Physiology-Lung Cellular and Molecular Physiology 298, no. 6 (June 2010): L768—L774. http://dx.doi.org/10.1152/ajplung.00353.2009.

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Vascular endothelial cell growth factor (VEGF) is a potent mitogen and permogen that increases in the plasma and decreases in the alveolar space in respiratory diseases such as acute respiratory distress syndrome (ARDS). This observation has led to controversy over the role of this potent molecule in lung physiology and disease. We hypothesized that some of the VEGF previously detected in normal lung may be of the anti-angiogenic family (VEGFxxxb) with significant potential effects on VEGF bioactivity. VEGFxxxb protein expression was assessed by indirect immunohistochemistry in normal and ARDS tissue. Expression of VEGFxxxb was also detected by immunoblotting in normal lung tissue, primary human alveolar type II (ATII) cells, and bronchoalveolar lavage (BAL) fluid in normal subjects and by ELISA in normal, “at risk,” and ARDS subjects. The effect of VEGF165 and VEGF165b on both human primary endothelial cells and alveolar epithelial cell proliferation was assessed by [3H]thymidine uptake. We found that VEGF165b was widely expressed in normal healthy lung tissue but is reduced in ARDS lung. VEGF121b and VEGF165b were present in whole lung, BAL, and ATII lysate. The proliferative effect of VEGF165 on both human primary endothelial cells and human alveolar epithelial cells was significantly inhibited by VEGF165b ( P < 0.01). These data demonstrate that the novel VEGFxxxb family members are expressed in normal lung and are reduced in ARDS. A specific functional effect on primary human endothelial and alveolar epithelial cells has also been shown. These data suggest that the VEGFxxxb family may have a role in repair after lung injury.
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Oltean, Sebastian, Christopher R. Neal, Athina Mavrou, Panisha Patel, Thomas Ahad, Chloe Alsop, Thomas Lee, et al. "VEGF165b overexpression restores normal glomerular water permeability in VEGF164-overexpressing adult mice." American Journal of Physiology-Renal Physiology 303, no. 7 (October 1, 2012): F1026—F1036. http://dx.doi.org/10.1152/ajprenal.00410.2011.

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Vascular endothelial growth factor (VEGF)-A, a family of differentially spliced proteins produced by glomerular podocytes, maintains glomerular filtration barrier function. The expression of VEGF molecules is altered in human nephropathy. We aimed to determine the roles of the angiogenic VEGF164 isoform, and the antiangiogenic VEGF165b isoform in mature, adult glomeruli in vivo using conditional, inducible transgenic overexpression systems in mice. Podocyte-specific VEGF164 overexpression (up to 100 days) was induced by oral administration of doxycycline to adult podocin-rtTA/TetO-VEGF164 double transgenic mice. The consequences of simultaneous overexpression of VEGF164 and VEGF165b were assessed in triple-transgenic podocin-rtTA/TetO-VEGF164/nephrin-VEGF165b mice. Persistent VEGF164 overexpression did not cause proteinuria but did increase glomerular ultrafiltration coefficient between days 3 and 7. Despite persistently increased VEGF164 levels, glomerular ultrafiltration coefficient normalized by day 14 and remained normal up to 100 days. Decreased subpodocyte space (SPS) coverage of the glomerular capillary wall accompanied increased glomerular hydraulic conductivity in VEGF164-overexpressing mice. The changes in glomerular ultrafiltration coefficient and SPS coverage induced by 7 days of overexpression of VEGF164 were not present in triple transgenic VEGF164 and VEGF165b overexpressing mice. These results indicate that 1) the adult mouse glomerulus is relatively resistant to induced VEGF164 overexpression. VEGF164 overexpression altered glomerular permeability but did not cause proteinuria in these mature, adult animals; 2) the SPS is a dynamic VEGF-responsive modulator of glomerular function; and 3) the balance of VEGF isoforms plays a critical role in the regulation of glomerular permeability. VEGF165b is capable of preventing VEGF164-induced changes in glomerular permeability and ultrastructure in vivo.
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Qiu, Y., M. Seager, A. Osman, J. Castle-Miller, H. Bevan, D. J. Tortonese, D. Murphy, et al. "Ovarian VEGF165b expression regulates follicular development, corpus luteum function and fertility." REPRODUCTION 143, no. 4 (April 2012): 501–11. http://dx.doi.org/10.1530/rep-11-0091.

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Angiogenesis and vascular regression are critical for the female ovulatory cycle. They enable progression and regression of follicular development, and corpora lutea formation and regression. Angiogenesis in the ovary occurs under the control of the vascular endothelial growth factor-A (VEGFA) family of proteins, which are generated as both pro-(VEGF165) and anti(VEGF165b)-angiogenic isoforms by alternative splicing. To determine the role of the VEGF165b isoforms in the ovulatory cycle, we measured VEGF165b expression in marmoset ovaries by immunohistochemistry and ELISA, and used transgenic mice over-expressing VEGF165b in the ovary. VEGF165b was expressed in the marmoset ovaries in granulosa cells and theca, and the balance of VEGF165b:VEGF165 was regulated during luteogenesis. Mice over-expressing VEGF165b in the ovary were less fertile than wild-type littermates, had reduced secondary and tertiary follicles after mating, increased atretic follicles, fewer corpora lutea and generated fewer embryos in the oviduct after mating, and these were more likely not to retain the corona radiata. These results indicate that the balance of VEGFA isoforms controls follicle progression and luteogenesis, and that control of isoform expression may regulate fertility in mammals, including in primates.
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Bates, David O., Paul J. Catalano, Kirsty E. Symonds, Alexander H. R. Varey, Pramila Ramani, Peter James O'Dwyer, Bruce J. Giantonio, Neal J. Meropol, Al Bowen Benson, and Steven J. Harper. "Predictive value of the antiangiogenic VEGF splice variant expression for bevacizumab efficacy in the phase III trial of bevacizumab and FOLFOX4 versus FOLFOX4 in previously treated patients with advanced colorectal cancer (ECOG E3200T2)." Journal of Clinical Oncology 30, no. 4_suppl (February 1, 2012): 545. http://dx.doi.org/10.1200/jco.2012.30.4_suppl.545.

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545 Background: Treatment of metastatic colorectal cancer (CRC) with bevacizumab (anti-VEGF) in combination with chemotherapy increases survival in a proportion of patients, but it is not possible a priori to predict which patients will receive benefit. The VEGF-A gene is alternatively spliced into two families by alternative splice site usage in exon 8. The pro-angiogenic (e.g. VEGF165) isoforms are generated by proximal splice site selection, and the anti-angiogenic (e.g. VEGF165b) by distal splice site selection. The relative levels of the isoforms vary in CRC. VEGF165b over-expression in mice inhibits bevacizumab treatment.We tested the hypothesis that survival would be better in patients with low VEGF165b levels on bevacizumab than placebo. Methods: To determine whether survival was better in patietns with low VEGF165b when treated with FOLFOX4+bevacizumab (Arm A) than FOLFOX4 + placebo (Arm B), 108 coded patient samples from the E3200 trial of FOLFOX4±bevacizumab (NCT NCT00897754 ) were successfully stained for VEGF-A165b and scored in well differentiated tissue relative to normal tissue blind to outcome. The VEGF165b expression relative to normal tissue was calculated. 108 cases were analysed for VEGF165b/Normal, 48 in arm A, 60 in Arm B. Results: Adjusted Cox Binary analysis of VEGF165b/Normal comparing staining ratio in bevacizumab versus placebo treated patients demonstrated significantly better survival for the less than median ratios (HR=0.28, p=0.0031, median progression free survival, 8.4 versus 5.1 months in placebo), whereas in the higher than median VEGF165b/Normal group there was no effect of bevacizumab (HR=0.96, median PFS, 11.9 compared with 11.0months). Results held after adjustment for other clinical and demographic features in proportional hazards regression modelling. Conclusions: In conclusion, these results indicate that low VEGF165b levels in well-differentiated tumours may predict response to bevacizumab.
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Bills, Victoria L., Julia Varet, Ann Millar, Steven J. Harper, Peter W. Soothill, and David O. Bates. "Failure to up-regulate VEGF165b in maternal plasma is a first trimester predictive marker for pre-eclampsia." Clinical Science 116, no. 3 (January 8, 2009): 265–72. http://dx.doi.org/10.1042/cs20080270.

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Pre-eclampsia is a pregnancy-related condition characterized by hypertension, proteinuria and endothelial dysfunction. VEGF165b, formed by alternative splicing of VEGF (vascular endothelial growth factor) pre-mRNA, inhibits VEGF165-mediated vasodilation and angiogenesis, but has not been quantified in pregnancy. ELISAs were used to measure means±S.E.M. plasma VEGF165b, sEng (soluble endoglin) and sFlt-1 (soluble fms-like tyrosine kinase-1). At 12 weeks of gestation, the plasma VEGF165b concentration was significantly up-regulated in plasma from women who maintained normal blood pressure throughout their pregnancy (normotensive group, 4.90±1.6 ng/ml; P&lt;0.01, as determined using a Mann-Whitney U test) compared with non-pregnant women (0.40±0.22 ng/ml). In contrast, in patients who later developed pre-eclampsia, VEGF165b levels were lower than in the normotensive group (0.467±0.209 ng/ml), but were no greater than non-pregnant women. At term, plasma VEGF165b concentrations were greater than normal in both pre-eclamptic (3.75±2.24 ng/ml) and normotensive (10.58 ng/ml±3.74 ng/ml; P&gt;0.1 compared with pre-eclampsia) pregnancies. Patients with a lower than median plasma VEGF165b at 12 weeks had elevated sFlt-1 and sEng pre-delivery. Concentrations of sFlt-1 (1.20±0.07 and 1.27±0.18 ng/ml) and sEng (4.4±0.18 and 4.1±0.5 ng/ml) were similar at 12 weeks of gestation in the normotensive and pre-eclamptic groups respectively. Plasma VEGF165b levels were elevated in pregnancy, but this increase is delayed in women that subsequently develop pre-eclampsia. In conclusion, low VEGF165b may therefore be a clinically useful first trimester plasma marker for increased risk of pre-eclampsia.
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Cui, Tai-Gen, Rebecca R. Foster, Moin Saleem, Peter W. Mathieson, David A. Gillatt, David O. Bates, and Steven J. Harper. "Differentiated human podocytes endogenously express an inhibitory isoform of vascular endothelial growth factor (VEGF165b) mRNA and protein." American Journal of Physiology-Renal Physiology 286, no. 4 (April 2004): F767—F773. http://dx.doi.org/10.1152/ajprenal.00337.2003.

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Despite production by podocytes of the proangiogenic molecule vascular endothelial growth factor-A (VEGF), the glomeruli are not sites of angiogenesis. We recently described mRNA expression of an inhibitory splice variant of VEGF (VEGF165b) in normal kidney (Bates DO, Cui TG, Doughty JM, Winkler M, Sugiono M, Shields JD, Peat D, Gillatt D, and Harper SJ. Cancer Res 62: 4123–4131, 2002). Available anti-VEGF antibodies do not distinguish stimulatory from inhibitory VEGF families. To assess the production of VEGF165 (stimulatory) and VEGF165b (inhibitory) isoforms by human podocytes, we examined both primary cultured and conditionally immortalized human podocytes using family- and isoform-specific RT-PCR. In addition, VEGF protein production was analyzed in podocytes, using isoform-specific double-strand small-interference RNAs (siRNA). RT-PCR demonstrated the production of VEGF189 mRNA by podocytes of both phenotypes. In contrast, on differentiation there was a splicing change from VEGF165 to VEGF165b mRNA. In addition, VEGF protein in the supernatant of conditionally immortalized, differentiated podocytes was reduced by VEGF165b siRNA to 20 ± 11% of the level of mock-transfected cells ( P < 0.01). No reduction was seen with mismatch siRNA. Moreover, there was no reduction in VEGF protein concentration in the supernatant of primary cultured, dedifferentiated human podocytes (109 ± 8% of mismatch siRNA, P > 0.1). In conclusion, differentiated but not dedifferentiated human podocytes secrete significant amounts of VEGF165b protein. It is possible that this may explain the paradox of high VEGF production in the glomerulus but no angiogenesis. Furthermore, the existence of this splicing switch in relation to podocyte phenotype suggests that alternative splicing of the VEGF pre-RNA is a regulated process that is open to manipulation and therefore could be a target for novel cancer therapies.
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Afkhami, Fatemeh, Yves Durocher, and Satya Prakash. "Investigation of Antiangiogenic Tumor Therapy Potential of Microencapsulated HEK293 VEGF165b Producing Cells." Journal of Biomedicine and Biotechnology 2010 (2010): 1–7. http://dx.doi.org/10.1155/2010/645610.

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To investigate the antiangiogenic potential of encapsulated VEGF165b producing HEK293 cells, Human Embryonic Kidney 293 (HEK293) cells were stably transfected to produce VEGF165b. Then they were encapsulated in alginate - polylysine -alginate (APA) microcapsules. VEGF165b productivity and viability of encapsulated cells were analyzed and compared with the non-encapsulated cells. Results showed that encapsulated cells proliferated and remained viable within the microcapsules throughout the 28-day period of the experiment. The quantity of VEGF165b increased from6.5±1.2 μg/ml at day 13 to13±0.96 μg/ml at day 16. Then it gradually dropped to5±1.2 μg/ml for the last 3 days period as measured at day 28. Production of VEGF165b from encapsulated and non-encapsulated cells was similar. The effect of VEGF165b harvested from encapsulated cells on Human Umbilical Vein Endothelial cells (HUVECs) proliferation were also examined.The same inhibitory effects on HUVECs proliferation was seen when the cells were incubated with a mixture of VEGF165b and a 2-fold VEGF165b or with VEGF165b and 2-fold excess VEGF165b released from encapsulated cells. Subcutaneous injection of microencapsulated VEGF165b producing cells in tumor site of nude mice resulted in the reduction of the number of vessels around the tumors.
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Kuppuswamy, Sivaraman, Brian H. Annex, and Vijay C. Ganta. "Targeting Anti-Angiogenic VEGF165b–VEGFR1 Signaling Promotes Nitric Oxide Independent Therapeutic Angiogenesis in Preclinical Peripheral Artery Disease Models." Cells 11, no. 17 (August 28, 2022): 2676. http://dx.doi.org/10.3390/cells11172676.

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Nitric oxide (NO) is the critical regulator of VEGFR2-induced angiogenesis. Neither VEGF-A over-expression nor L-Arginine (NO-precursor) supplementation has been effective in helping patients with Peripheral Artery Disease (PAD) in clinical trials. One incompletely studied reason may be due to the presence of the less characterized anti-angiogenic VEGF-A (VEGF165b) isoform. We have recently shown that VEGF165b inhibits ischemic angiogenesis by blocking VEGFR1, not VEGFR2 activation. Here we wanted to determine whether VEGF165b inhibition using a monoclonal isoform-specific antibody against VEGF165b vs. control, improved perfusion recovery in preclinical PAD models that have impaired VEGFR2-NO signaling, including (1) type-2 diabetic model, (2) endothelial Nitric oxide synthase-knock out mice, and (3) Myoglobin transgenic mice that have impaired NO bioavailability. In all PAD models, VEGF165b inhibition vs. control enhanced perfusion recovery, increased microvascular density in the ischemic limb, and activated VEGFR1-STAT3 signaling. In vitro, VEGF165b inhibition vs. control enhanced a VEGFR1-dependent endothelial survival/proliferation and angiogenic capacity. These data demonstrate that VEGF165b inhibition induces VEGFR1-STAT3 activation, which does not require increased NO to induce therapeutic angiogenesis in PAD. These results may have implications for advancing therapies for patients with PAD where the VEGFR2-eNOS-NO pathway is impaired.
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Catena, Raúl, Leyre Larzabal, Marta Larrayoz, Eva Molina, Jose Hermida, Jackeline Agorreta, Ramon Montes, Ruben Pio, Luis M. Montuenga, and Alfonso Calvo. "VEGF121b and VEGF165b are weakly angiogenic isoforms of VEGF-A." Molecular Cancer 9, no. 1 (2010): 320. http://dx.doi.org/10.1186/1476-4598-9-320.

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Dissertations / Theses on the topic "VEGF165b"

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Niederhäuser, Monika. "Production and characterization of mutant VEGF165 and VEGF165b." Zürich : ETH, Eidgenössische Technische Hochschule Zürich, Departement Chemie und Angewandte Biowissenschaften, 2005. http://e-collection.ethbib.ethz.ch/show?type=dipl&nr=177.

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Dersch, Rick [Verfasser], and Wolf A. [Akademischer Betreuer] Lagrèze. "Wirkung von VEGF165b auf die gesunde und die ischämische Netzhaut der Ratte." Freiburg : Universität, 2011. http://d-nb.info/112345857X/34.

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Afkhami, Zarreh Fatemeh. "Delivery of IFNa and VEGF165b by microencapsulated cells: preparation and «in vitro» analysis." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=66849.

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ABSTRACT The pivotal role of angiogenesis in the growth and spread of all solid tumors has driven the cancer research on applying antiangiogenic factors to suppress formation of new blood vessels in order to prevent or slow tumor growth. Glycoproteins, Interferon alpha (IFNα and VEGF165b are of particular interest in this study. IFNα is a multifunctional cytokine with many physiological effects including antiangiogenesis effects. VEGF165b is a competitive antagonist of the Vascular Endothelial Growth Factor (VEGF) receptor and has been reported to successfully inhibit angiogenesis. The thesis goal is to develop a system for simultaneous production of IFNα2b (IFNα) and VEGF165b and targeted delivery to enhance their antiangiogenic properties. For this purpose, HEK293 cells were developed to produce IFNα and VEGF165b simultaneously. The potential of a stable HEK293 cell line producing IFNα or VEGF165b to continuously deliver IFNα or VEGF165b after encapsulation in alginate-poly-l-lysine-alginate (APA) microcapsules was evaluated. For a better delivery system, co-encapsulation of HEK293 VEGF165b producing cells and HEK293 IFNα producing cells or a mixture of encapsulated HEK293 cells producing either IFNα or VEGF165b were studied. Attempts were also made to increase the bioactivity (pharmacodynamic) of IFNα by modifying its O-glycosylation to an N-glycosylation site and of VEGF165b by increasing its sialylation level. The bioactivity was investigated in experimental rats. The results suggest that one cell line, HEK293, can produce IFNα and VEGF165b simultaneously. This process has the advantage of ease of manipulation and low cost but is somewhat limited by the fact that production of IFNα and VEGF165b cannot be controlled. Microencapsulation of IFNα or VEGF165b producing cells demonstrates that encapsulated cells grow and remain viable within the microcapsules. The IFNα and VEGF165b released
RÉSUMÉLe IFNα est une cytokine multifonctionnelle avec plusieurs effets physiologiques incluant l'antiangiogenèse effets tandis que le VEGF165b est un antagoniste concurrentiel du récepteur de Vascular Endothelial Growth Factor (VEGF) et empêche avec succès l'angiogenèse. La thèse a pour but de développer un système pour la production simultanée du IFNα et du VEGF165b, de plus, que la livraison soit ciblée pour augmenter les propriétés antiangiogéniques. À cette fin, les cellules HEK293 ont été génétiquement modifiées pour produire simultanément l'IFNα et le VEGF165b. Le potentiel d'une lignée cellulaire HEK293 stable, produisant simultanément le IFNα ou VEGF165b pour livrer en perpétuité le IFNα et VEGF165b après l'encapsulation dans des microcapsules composé de l'alginate-poly-l-lysine-alginate (APA) a été évalué. Pour apporté des améliorations au système, deux mélanges ont été évalué. La co-encapsulation de cellules HEK293 produisant le VEGF165b et de cellules de HEK293 produisant IFNα et un mélange deux types de cellules encapsulées séparément ont été étudiés. Des tentatives ont été également accomplies pour augmenter leur bioactivité (pharmacodynamic) du IFNα en modifiant son O-glycosylation à un emplacement de N-glycosylation et de VEGF165b en augmentant son niveau de sialylation. La bioactivité a été étudiée chez les rats expérimentaux. Les résultats suggèrent que les cellules, HEK293, puissent produire l'IFNα et le VEGF165b simultanément. Ce processus a l'avantage de facilité la manipulation et de maintenir les coûts bas mais est légèrement limité par le fait que la production du d'IFNα et du VEG165Fb ne peut pas être contrôlée. Le microencapsulation de cellules produisant le IFNα ou VEGF165b démontrent que les cellules encapsulées se développent tout en retenant leur capacités de synthèses et demeurent viables d
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Kermani, Pouneh. "Rôle de VEGF165 dans l'ischémie myocardique et lors de radiation ionisante des cellules endothéliales /." [Montréal] : Université de Montréal, 2001. http://wwwlib.umi.com/cr/umontreal/fullcit?pNQ65373.

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Thèse (Ph. D.)--Université de Montréal, 2001.
"Thèse présentée à la faculté des études supérieures en vue de l'obtention du grade de philosophiae doctor (Ph. D.) en biologie moléculaire." Version électronique également disponible sur Internet.
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Abou, faycal Chérine. "Le sVEGFR1 : quel rôle dans la réponse aux thérapies antiangiogéniques dans les carcinomes pulmonaires squameux ?" Thesis, Université Grenoble Alpes (ComUE), 2016. http://www.theses.fr/2016GREAV022/document.

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Le VEGF-A joue un rôle clé au cours de l’angiogenèse physiologique mais aussi de la néo-vascularisation tumorale essentielle à la croissance des tumeurs malignes. Le VEGF-A et ses récepteurs (VEGFR1/2) représentent une cible de première importance pour le développement de thérapies anti-tumorales, et un certain nombre de médicaments anti-angiogéniques (AAG) inhibant le VEGF-A ou ses récepteurs sont actuellement utilisés en clinique dans le traitement des carcinomes pulmonaires. Parmi les thérapies anti-angiogéniques ciblant le VEGF-A, on peut lister soit l’anticorps monoclonal anti-VEGF Bevacizumab (BVZ) ou bien les inhibiteurs pharmacologiques du domaine tyrosine kinase des VEGFR: les VEGFR-TKI. Seuls les patients porteurs d’adénocarcinomes pulmonaires peuvent bénéficier de thérapies AAG, les patients porteurs de carcinomes squameux présentant de sévères complications (hémorragies pulmonaires). Le sVEGFR1, est un variant tronqué du VEGFR1 qui ne contient que les premiers six motifs N-terminaux extracellulaires de type Ig du domaine extracellulaire et il est dépourvu des domaines transmembranaire et tyrosine kinase. Le sVEGFR1 a éte initialement considéré comme un facteur anti-angiogénique qui neutralise les fonctions du VEGF-A dans les cellules endothéliales. Les hauts niveaux ont été corrélés avec un mauvais pronostic et une mauvaise réponse aux thérapies dans plusieurs types de cancer. Nous avons montré in vitro dans 4 lignées cellulaires de SCC que le bevacizumab, ainsi que les inhibiteurs VEGF-TKI (Semaxanib, KI8751) augmentent les niveaux intra- et extra-cellulaires du sVEGFR1. Nous avons confirmé ces résultats in vivo dans des modèles murins de xénogreffes squameux induits par NCTU. De façon intérssante, l’augmentation du sVEGFR1 en réponse aux thérapies anti-angiogénique est spécifique aux modèles squameux et n’a pas été observée dans les modèles d’adénocarcinomes in vitro et in vivo. Sur le plan moléculaire, nous avons montré que le VEGF165 par l’intermédiaire de SOX2 régule l’expression du sVEGFR1 en réponse aux thérapiesAAG. De plus, nous avons identifié une boucle autocrine 1 intégrine / VEGFR1 / VEGFR2 par laquelle sVEGFR1 contrôle différentiellement la prolifération cellulaire et la survie, permettant notamment de distinguer les cellules SCC sensibles ou résistantes aux thérapies AAG. Enfin, dans une série de 77 cancers bronchiques non à petites cellules, nous avons montré que 11% et 44% des patients SCC expriment de bas ou de hauts nivaux de sVEGFR1 respectivement. Les hauts niveaux ont été corrélés avec des stades pTNM avancés. Dans l'ensemble, nos résultats sont la première preuve que les thérapies AAG augmentent l'expression du sVEGFR1 dans les cellules SCC. En outre, nos données mettent en évidence une fonction pro-tumorale inattendue de sVEGFR1 grâce à l'activation d'une boucle autocrine VEGFR/ β1 intégrine. Ces résultats pourraient aider à comprendre pourquoi les SCC répondent différemment aux AAG que les ADC et d'identifier les patients SCC qui pourraient etre éligibles à ces thérapies
Vascular endothelial growth factors (VEGFs) and their receptors are regulators of physiological and pathological angiogenesis. In patients with squamous cell lung carcinoma (SCC), clinical trials evaluating anti-angiogenic therapies (AAG) have failed to identify strong benefits. Rather, these patients are at higher risk of bleeding complications when exposed to Bevacizumab (BVZ), a humanized monoclonal anti-VEGF-A antibody. The soluble VEGF receptor-1, namely sVEGFR1, is a truncated version of the cell membrane-spanning VEGFR1 that only retains the first six N-terminal Ig-like extracellular motifs of VEGFR1 owing to alternative splicing of its pre-mRNA. As a consequence, sVEGFR1 is mainly viewed as an anti-angiogenic factor that counteracts VEGF-A functions on endothelial cells. Moreover, high levels of sVEGFR1 were correlated with bad prognosis and bad response to therapies in many cancer types. Using various SCC cell lines, we showed that Bevacizumab as well as VEGFR-Tyrosine Kinase Inhibitors (Semaxanib, KI8751) increase the intra- and extra-cellular levels of sVEGFR1. We confirmed this up-regulation in NCTU-induced SCC murine tumorgrafts models treated with VEGFR-TKI (sunitinib) or anti-VEGFR2 (DC101). Of note, this effect was never observed in the lung adenocarcinoma histological sub-type (ADC), using either cell lines or a mouse model treated in the same conditions. At the molecular level, we identified the VEGF165 and SOX2 proteins as crucial upstream regulators of sVEGFR1 in response to AAG. Moreover, we unraveled an original and SOX2 proteins as crucial upstream regulators of sVEGFR1 in response to AAG. Moreover, we unraveled an original ines or a mouse model treato discriminate between AAG-sensitive or -resistant SCC cells. Finally, in a series of 77 Non Small Cell Lung Carcinoma, we provided the first description of a differential pattern of sVEGFR1 expression with 11% and 44% of SCC exhibiting no or high expression respectively, high levels of sVEGFR1 being correlated with advanced pTNM stages. As a whole, our results provide the first evidence that AAG therapies upregulate sVEGFR1 expression in SCC cells. In addition, our data highlight an unexpected pro-tumoral function of sVEGFR1 through the activation of a beta 1 integrin-dependent VEGFR autocrine loop. These results might help to understand why SCC are less responsive to anti-angiogenic drugs than ADC and to identify SCC patients eligible to these therapies
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Hillenbrand, Matthias. "Verbesserte Nervenregeneration durch adenovirale Gentherapie mit VEGF165 im Modell der geburtstraumatischen Plexusparese an der Ratte." Diss., Ludwig-Maximilians-Universität München, 2014. http://nbn-resolving.de/urn:nbn:de:bvb:19-174979.

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Völschow, Chiara Catharina [Verfasser]. "Präfabrikation von vaskularisierten Transplantaten mittels rhBMP-2 und VEGF165 im Omentum majus des Kaninchens / Chiara Catharina Völschow." Kiel : Universitätsbibliothek Kiel, 2017. http://d-nb.info/1149512776/34.

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Krilleke, D. "Structural and functional analysis of the heparin-binding domain of VEGF164." Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1444908/.

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Several of the multitude of functions attributed to Vascular Endothelial Growth Factor-A (VEGF-A) are coordinated by its various isoforms, which are generated as a result of alternative splicing from a single gene. Despite the fact that the VEGF isoforms exhibit distinct biochemical properties, little has been done to clarify their functions and their contributions to physiological and pathological processes. In this thesis I describe the biochemical and biological characterization of the heparin-binding domain of mouse VEGF 164 through structure-function analysis. To investigate the functional significance of heparin binding, mutations were introduced into exon 7 of VEGF 164 to identify essential residues for heparin binding. Three key amino acids involved in this interaction were identified. Mutants with alterations in these amino acids were unable to bind heparin and were compromised in their ability to bind to cell-surface heparan sulfate. These mutants, however, retained wild-type like potency in inducing tissue factor expression in vitro and microvessel growth ex vivo, and maintained the capacity to bind to the receptors neuropilin-1, VEGFR-1, and VEGFR-2. A second goal of this work was to better define the role of VEGF 164 in mediating inflammatory processes during pathological vascularization of the retina. Analysis of VEGF 164-deficient (VEGF1ZU/ iao) mice subjected to neovascularization-inducing conditions and rats injected intravitreally with recombinant VEGF variants demonstrated that endogenous and exogenous VEGF 164 increases leukocyte adhesiveness to retinal vessels compared to the non-heparin-binding isoform, VEGF 120. Interestingly, the three basic residues that confer heparin binding of VEGF 164, appear to be critical for its pro inflammatory activity, but not for its angiogenic activity. In addition, both mutants (and VEGF 120) exhibited a reduced affinity for VEGFR-1, a leukocyte-expressed receptor that mediates VEGF-induced migration. Results of in vivo experiments using P1GF, VEGF-E, as well as a VEGFR-1 neutralizing antibody, further demonstrate a role for VEGFR-1 in retinal leukostasis.
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Brunet, de la Grange Philippe. "Régulation de l'hématopoïèse par les basses concentrations d'oxygène : rôles de l'antigène CD34 et du facteur de croissance VEGF165." Bordeaux 2, 2004. http://www.theses.fr/2004BOR21093.

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L'hématopoïèse, processus de production des cellules sanguines à partir des cellules souches, est notamment régulée par les concentrations d'O2 médullaires comprises entre 0 à 5 % (hypoxie). Nous avons établi des liens entre des facteurs intrinsèques à la cellule impliqués dans le processus de différenciation (antigène CD34) et leur sensibilité à l'hypoxie, et étudié les effets sur l'hématopoïèse de facteurs inductibles par l'hypoxie (Vascular Endothelial Growth Factor, VEGF). La culture de cellules hématopoiétiques CD34+ à 1 % d'O2 augmente ou stabilise l'expression du gène cd34 qui diminue à 20 % d'O2. Le maintien prolongé de cette expression associé à une expression membranaire durable de la protéine sont corrélés avec le statut immature des cellules. D'autre part, le VEGF165 permet la survie de cellules souches murines en culture liquide à 1 % d'O2. Ainsi l'hypoxie freine la différenciation des cellules souches par l'expression du gène cd34 et favorise leur survie par le VEGF165
Hematopoiesis, the process of mature blood production from stem cells, is in part regulated by bone marrow oxygen concentrations, which vary from 0 to 5 % (hypoxia). We studied in this work the relationships between cell intrinsic factors involved in the maturation process (CD34 antigen) and their sensitivity to hypoxia, and the effects of molecules inducible by hypoxia (Vascular Endothelial Growth Factor, VEGF) on hematopoiesis. We showed that cultures of CD34+ cells at 1 % O2 induce or stabilize the cd34 gene expression that decreases at 20 % O2. The prolonged maintenance of this expression associated with the long-lasting membrane expression of the protein were correlated with the primitiveness of cells. We also showed that VEGF165 led to the survival of murine stem cells cultured at 1 % O2. This work suggests that hypoxia slows down the differentiation of stem cells by inducing cd34 gene expression, and favours their survival through VEGF165
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Lambert, Sophie. "Rôle majeur de la neuropiline-1 dans le mécanisme d'entrée du HTLV-1 : le récepteur du HTLV-1 : un ménage à trois ?" Paris 6, 2008. http://www.theses.fr/2008PA066061.

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HTLV-1(Human T cell Leukemia Virus type 1) est un rétrovirus oncogène qui infecte majoritairement les lymphocytes T CD4+. Il est transmis par contact entre deux cellules, via une synapse virale. L’entrée du virus dans une cellule cible met en jeu deux partenaires : les glycoprotéines d’enveloppe virales (Env) et plusieurs récepteurs cellulaires. Un premier récepteur a été décrit récemment : le transporteur de glucose de type 1 (Glut-1). Il a ensuite été montré que les Héparanes Sulfates ProtéoGlycanes (HSPGs) étaient un constituant essentiel du complexe récepteur, et interviennent dans les étapes précoces du mécanisme d’entrée. Pour notre part, nous avons démontré que la neuropiline-1 (NRP-1), récepteur de la sémaphorine 3A et du VEGF165 est également un constituant du HTLV-1 (article 1). Un des complexes récepteurs du VEGF165 est constitué de la NRP-1, des HSPGs et du récepteur de type 2 du VEGF. Le VEGF165 et la NRP-1 sont tous deux capables de lier les héparanes sulfates (HS), le VEGF165 se lie majoritairement à la NRP-1 de façon HS-dépendante. Néanmoins, une interaction directe du VEGF165 à la NRP-1, impliquant les derniers résidus du VEGF165, existe également. En nous basant sur le modèle du VEGF165, nous avons montré que les HS et la NRP-1 coopèrent dans le processus d’entrée. Par ailleurs, nous avons mis en évidence que l’Env partage un motif d’homologie avec le VEGF165 qui lui permet également de s’associer directement à la NRP-1. L’ensemble de ce travail nous permet de proposer un modèle d’entrée complètement nouveau impliquant les trois molécules préalablement décrites et un mimétisme moléculaire entre un domaine du VEGF165 et l’Env du HTLV-1 (article 2).
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Book chapters on the topic "VEGF165b"

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Spanholtz, T., S. Söllner, C. Niedworok, A. Maichle, W. Lindenmaier, S. Krüger, B. Stöcklhuber, P. Mailänder, and H. G. Machens. "PDGF-BB stabilisiert VEGF165-induzierte »leaky vessels« nach zell-basiertem Gentransfer in vivo." In Chirurgisches Forum 2006, 383–85. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/3-540-34668-6_131.

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Maichle, A., C. Niedworok, T. Spanholtz, W. Lindenmaier, S. Herbort-Brand, S. Krüger, B. Stöckelhuber, B. D. Krapohl, P. Mailänder, and H. G. Machens. "Timing und Target der temporären Genexpression von VEGF165 in einem ischämischen Lappenmodell der Ratte." In Deutsche Gesellschaft für Chirurgie, 17–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18547-2_6.

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Spanholtz, T., C. Niedworok, A. Maichle, W. Lindenmaier, S. Krüger, B. Stöckelhuber, P. Mailänder, and H. G. Machens. "Synergistische therapeutische Effekte von bFGF und VEGF165 nach Transplantation isogener adenoviral transfizierter Fibroblasten im ischämischen Lappenmodell der Ratte." In Deutsche Gesellschaft für Chirurgie, 421–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2004. http://dx.doi.org/10.1007/978-3-642-18547-2_129.

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Vieira, Joaquim Miguel, Quenten Schwarz, and Christiana Ruhrberg. "Role of the Neuropilin Ligands VEGF164 and SEMA3A in Neuronal and Vascular Patterning in the Mouse." In Vascular Development, 230–37. Chichester, UK: John Wiley & Sons, Ltd, 2007. http://dx.doi.org/10.1002/9780470319413.ch18.

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Conference papers on the topic "VEGF165b"

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Afkhami, Fatemeh, Satya Prakash, and Yves Durocher. "Local delivery of VEGF165b and IFNα by microencapsulated cells as potential antiangiogenic therapy." In 2009 IEEE 35th Annual Northeast Bioengineering Conference. IEEE, 2009. http://dx.doi.org/10.1109/nebc.2009.4967686.

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Guenthner-Biller, MM, A. Rademacher, D. Mayr, V. Engelstädter, K. Friese, U. Jeschke, and B. Rack. "OT2-03-05: Evaluation of the Prevalence and Prognostic Significance of VEGF165b in Breast Cancer Patients Compared to Healthy Women." In Abstracts: Thirty-Fourth Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 6‐10, 2011; San Antonio, TX. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/0008-5472.sabcs11-ot2-03-05.

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Monks, Anne, Curtis D. Hose, and James H. Doroshow. "Abstract 2853: Sunitinib induces anti-angiogenic splice-variant VEGF165b through induction of CLK1 and CLK4 kinases in prostate cell line DU-145." 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.am2011-2853.

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Gounis, Matthew J., Baruch B. Lieber, Keith A. Webster, Bernard J. Wasserlauf, Howard M. Prentice, and Ajay K. Wakhloo. "Angiographic Quantification of Angiogenesis." In ASME 2003 International Mechanical Engineering Congress and Exposition. ASMEDC, 2003. http://dx.doi.org/10.1115/imece2003-43196.

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Therapeutic angiogenesis is the attempt to increase vascular density by means of an exogenously administered proangiogenic agent and offers a potential treatment for diseases associated with tissue ischemia. Vascular endothelial growth factor (VEGF) expressed by gene therapy has been shown to be a potent stimulator of angiogenesis and to improve the function of ischemic tissues in patients [Isner, 1998]. Unregulated gene therapy is disconcerting since there is no assurance that the treatment will target the ischemic territory. A new regulated adeno-associated viral vector expressing VEGF165 that is conditionally silenced has been developed by one of the authors (KAW). The transgene expression is regulated by silencing the genes in the absence of the disease and at the same time having strong and local activation in the presence of the disease. The purpose of this work is to establish protocols and techniques to quantify the efficacy of therapeutic angiogenesis. The initial phase of this research involves assessment of angiogenesis using an unregulated, adenoviral vector that is encoded to express VEGF165. Using the rabbit hind limb ischemia model, angiography was performed on animals that were given the proangiogenic treatment and on a sham group, in which phosphate buffered saline (PBS) was injected. Angiographic contrast intensity curves were obtained, modeled, and the optimized model parameters provided insight into flow characteristics within the targeted vascular bed. In the second phase of the project the conditionally silent vector will be employed using the developed protocols and methods of the first phase to afford comparisons with the previous groups.
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Zhang, Xiaofeng, Tielian Liu, Weihua Sheng, Yufeng Xie, Jingcheng Miao, and Jicheng Yang. "Enhanced Capillary Formation by Transplanted Ad-VEGF165 Transgenic Epithelial Cells on Silk Fibroin Films." In 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5517505.

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Clifford, Rachel L., Alison E. John, William R. Coward, C. E. Brightling, and Alan J. Knox. "Aberrant Histone Methylation And SP1 Association Are Responsible For VEGF165a Hypersecretion From Asthmatic Airway Smooth Muscle Cells (ASMCS)." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4057.

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Kim, Byeong Mo, Young Ae Joe, and Sung Hee Hong. "Abstract 1289: The recombinant kringle domain of urokinase plasminogen activator (uPA) inhibits VEGF165-induced proliferation of HUVEC cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1289.

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Tu, Juan, Qian Li, Chunbing Zhang, and Dong Zhang. "Enhancement effect of ultrasound-induced microbubble cavitation on branched polyethylenimine-mediated Vascular Endothelial Growth Factor 165 (VEGF165)transfection." In ICA 2013 Montreal. ASA, 2013. http://dx.doi.org/10.1121/1.4800028.

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