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Journal articles on the topic 'VEGF165b'

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Published: 10 March 2023

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1

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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2

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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3

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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4

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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5

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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6

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<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>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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7

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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8

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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9

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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10

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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11

Bevan, H. S., J. Woolard, S. J. Harper, and D. O. Bates. "OC21 VEGF165b INHIBITS VEGF165 MEDIATED VEGF-R2 PHOSPHORYLATION AND AKT PHOSPHORYLATION." Microcirculation 11, no. 6 (September 2004): 536. http://dx.doi.org/10.1080/10739680490488319.

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12

Peiris-Pagès, Maria. "The role of VEGF165b in pathophysiology." Cell Adhesion & Migration 6, no. 6 (November 17, 2012): 561–68. http://dx.doi.org/10.4161/cam.22439.

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13

Bates, David O., Philip P. MacMillan, Joseph G. Manjaly, Yan Qiu, Sarah J. Hudson, Heather S. Bevan, Alyson J. Hunter, et al. "The endogenous anti-angiogenic family of splice variants of VEGF, VEGFxxxb, are down-regulated in pre-eclamptic placentae at term." Clinical Science 110, no. 5 (April 11, 2006): 575–85. http://dx.doi.org/10.1042/cs20050292.

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PET (pre-eclamptic toxaemia) has recently been linked with alterations in production of a VEGFR1 [VEGF (vascular endothelial growth factor) receptor 1] splice variant that acts as a circulating inhibitor. We have recently described a family of naturally occurring splice variants of VEGF, termed VEGFxxxb, that also appear to act as inhibitors of conventional VEGFxxx-mediated angiogenesis. To determine whether alteration in splicing of VEGF–VEGFR family members extended beyond VEGFR1, we investigated the effect of pre-eclampsia on placental VEGFxxxb mRNA and protein expression. VEGFxxx and VEGFxxxb mRNA and protein were both found in normal human term placentae. VEGFxxx protein formed the majority of the total VEGF protein (980±195 pg/mg), whereas VEGFxxxb (11.5 pg/mg) was found to form a small part of the total VEGF protein expression (1.5±0.24%). Evidence for VEGF165b, VEGF121b and VEGF145b expression was found. In pre-eclamptic placentae, there was a significant down-regulation of VEGFxxxb isoforms, but a small up-regulation of VEGFxxx isoforms. In normal placenta VEGFxxxb and VEGFxxx concentrations were positively correlated (r=0.69, P<0.02), whereas in pre-eclamptic placentae, there was a significant negative correlation between VEGFxxxb and VEGFxxx protein expression (r=−0.8, P<0.02), indicating that there was a significant uncoupling of the splicing regulation of the VEGF isoforms. Combined with previous studies showing increased soluble VEGFR1 isoforms in human pre-eclampsia, these data suggest that there may be a common mechanism in pre-eclampsia that involves dysregulation of mRNA splicing of members of the VEGF–VEGFR axis.

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Hua, Jing, Christine Spee, Satoru Kase, Emma S. Rennel, Anette L. Magnussen, Yan Qiu, Alex Varey, et al. "Recombinant Human VEGF165b Inhibits Experimental Choroidal Neovascularization." Investigative Opthalmology & Visual Science 51, no. 8 (August 1, 2010): 4282. http://dx.doi.org/10.1167/iovs.09-4360.

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15

Qiu, Yan, Joanne Ferguson, Sebastian Oltean, Chris R. Neal, Amit Kaura, Heather Bevan, Emma Wood, et al. "Overexpression of VEGF165b in Podocytes Reduces Glomerular Permeability." Journal of the American Society of Nephrology 21, no. 9 (August 5, 2010): 1498–509. http://dx.doi.org/10.1681/asn.2009060617.

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Clegg, Lindsay E., Vijay C. Ganta, Brian H. Annex, and Feilim Mac Gabhann. "Systems Pharmacology of VEGF165b in Peripheral Artery Disease." CPT: Pharmacometrics & Systems Pharmacology 6, no. 12 (November 28, 2017): 833–44. http://dx.doi.org/10.1002/psp4.12261.

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17

Díaz, Raquel, Cristina Peña, Javier Silva, Yolanda Lorenzo, Vanesa García, José M. García, Antonio Sánchez, et al. "p73 isoforms affect VEGF, VEGF165b and PEDF expression in human colorectal tumors: VEGF165b downregulation as a marker of poor prognosis." International Journal of Cancer 123, no. 5 (September 1, 2008): 1060–67. http://dx.doi.org/10.1002/ijc.23619.

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Gopi, S., M. H-Zadeh, C. Sen, S. Harper, D. Bates, and D. Gillatt. "SCHU-01: VEGF165b, an Inhibitory Splice Variant of VEGF165 in Transitional Cell Carcinoma of the Bladder: In Vivo Expression." Urology 72, no. 5 (November 2008): S3. http://dx.doi.org/10.1016/j.urology.2008.08.004.

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19

Krishnasamy, Sundar, Vidya Ravi, Barathi Rajaraman, Senthil Kumar Thulasingam, C. S. Dhevasena, Atima Pathak, Krishnan Swaminathan, et al. "Role of VEGF165b/VEGFTOTAL ratio in gestational diabetes mellitus." Gynecological Endocrinology 35, no. 9 (April 9, 2019): 811–14. http://dx.doi.org/10.1080/09513590.2019.1595576.

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20

Woolard, Jeanette, Wen-Ying Wang, Heather S. Bevan, Yan Qiu, Lucia Morbidelli, Rowan O. Pritchard-Jones, Tai-Gen Cui, et al. "VEGF165b, an Inhibitory Vascular Endothelial Growth Factor Splice Variant." Cancer Research 64, no. 21 (November 1, 2004): 7822–35. http://dx.doi.org/10.1158/0008-5472.can-04-0934.

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21

Carter, Joanne J., Amanda J. Wheal, Stephen J. Hill, and Jeanette Woolard. "Effects of receptor tyrosine kinase inhibitors on VEGF165a- and VEGF165b-stimulated gene transcription in HEK-293 cells expressing human VEGFR2." British Journal of Pharmacology 172, no. 12 (April 10, 2015): 3141–50. http://dx.doi.org/10.1111/bph.13116.

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Vanderstraeten, Jessica, Bjorn Baselet, Jasmine Buset, Naziha Ben Said, Christine de Ville de Goyet, Marie-Christine Many, Anne-Catherine Gérard, and Hanane Derradji. "Modulation of VEGF Expression and Oxidative Stress Response by Iodine Deficiency in Irradiated Cancerous and Non-Cancerous Breast Cells." International Journal of Molecular Sciences 21, no. 11 (May 31, 2020): 3963. http://dx.doi.org/10.3390/ijms21113963.

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Breast cancer remains a major concern and its physiopathology is influenced by iodine deficiency (ID) and radiation exposure. Since radiation and ID can separately induce oxidative stress (OS) and microvascular responses in breast, their combination could additively increase these responses. Therefore, ID was induced in MCF7 and MCF12A breast cell lines by medium change. Cells were then X-irradiated with doses of 0.05, 0.1, or 3 Gy. In MCF12A cells, both ID and radiation (0.1 and 3 Gy) increased OS and vascular endothelial growth factor (VEGF) expression, with an additive effect when the highest dose was combined with ID. However, in MCF7 cells no additive effect was observed. VEGF mRNA up-regulation was reactive oxygen species (ROS)-dependent, involving radiation-induced mitochondrial ROS. Results on total VEGF mRNA hold true for the pro-angiogenic isoform VEGF165 mRNA, but the treatments did not modulate the anti-angiogenic isoform VEGF165b. Radiation-induced antioxidant response was differentially regulated upon ID in both cell lines. Thus, radiation response is modulated according to iodine status and cell type and can lead to additive effects on ROS and VEGF. As these are often involved in cancer initiation and progression, we believe that iodine status should be taken into account in radiation prevention policies.

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Afkhami, Fatemeh, Yves Durocher, and Satya Prakash. "Microencapsulated Mammalian Cells for Simultaneous Production of VEGF165b and IFNα." Artificial Cells, Blood Substitutes, and Biotechnology 40, no. 1-2 (January 31, 2012): 1–6. http://dx.doi.org/10.3109/10731199.2011.560120.

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Chen, Lingdan, Mingjie Yuan, and Tao Wang. "VEGF165b elevation in pulmonary arterial hypertension patients, causative or adaptive?" International Journal of Cardiology 256 (April 2018): 31. http://dx.doi.org/10.1016/j.ijcard.2017.11.028.

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Schumacher, Valérie Anne, Stefanie Jeruschke, Frank Eitner, Jan Ulrich Becker, Gerald Pitschke, Yasemin Ince, Jeffrey H. Miner, et al. "Impaired Glomerular Maturation and Lack of VEGF165b in Denys-Drash Syndrome." Journal of the American Society of Nephrology 18, no. 3 (January 31, 2007): 719–29. http://dx.doi.org/10.1681/asn.2006020124.

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Yoshihisa, Akiomi, Satoshi Suzuki, and Yasuchika Takeishi. "VEGF165b elevation in pulmonary arterial hypertension patients, causative or adaptive? -Reply-." International Journal of Cardiology 256 (April 2018): 32. http://dx.doi.org/10.1016/j.ijcard.2017.11.042.

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27

Rennel, Emma S., Maryam A. Hamdollah-Zadeh, Edward R. Wheatley, Anette Magnussen, Yvonne Schüler, Sara P. Kelly, Ciara Finucane, et al. "Recombinant human VEGF165b protein is an effective anti-cancer agent in mice." European Journal of Cancer 44, no. 13 (September 2008): 1883–94. http://dx.doi.org/10.1016/j.ejca.2008.05.027.

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Bills, Victoria, Peter Soothill, and Dave Bates. "The role of VEGF165b in trophoblast survival – Implications for pre-eclampsia pathophysiology." Placenta 35, no. 9 (September 2014): A73. http://dx.doi.org/10.1016/j.placenta.2014.06.237.

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Zhang, Huiyong, Enchao Jia, Wenjiao Xia, Tanyu Lv, Chengui Lu, Zhenping Xu, and Wuling Zhu. "Utilizing VEGF165b mutant as an effective immunization adjunct to augment antitumor immune response." Vaccine 37, no. 15 (April 2019): 2090–98. http://dx.doi.org/10.1016/j.vaccine.2019.02.055.

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30

Pritchard Jones, R., E. Rennel, S. Harper, A. Orlando, and D. Bates. "The endogenous antiangiogenic molecule VEGF165b inhibits the proliferation of A375 melanoma in vitro." Melanoma Research 16, Supplement 1 (September 2006): S8—S9. http://dx.doi.org/10.1097/00008390-200609001-00013.

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Bills, VL, AH Salmon, SJ Harper, TG Overton, CR Neal, B. Jeffery, PW Soothill, and DO Bates. "Impaired vascular permeability regulation caused by the VEGF165b splice variant in pre-eclampsia." BJOG: An International Journal of Obstetrics & Gynaecology 118, no. 10 (June 14, 2011): 1253–61. http://dx.doi.org/10.1111/j.1471-0528.2011.02925.x.

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32

Rennel, E. S., E. Waine, H. Guan, Y. Schüler, W. Leenders, J. Woolard, M. Sugiono, et al. "The endogenous anti-angiogenic VEGF isoform, VEGF165b inhibits human tumour growth in mice." British Journal of Cancer 98, no. 7 (March 18, 2008): 1250–57. http://dx.doi.org/10.1038/sj.bjc.6604309.

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Jiang, Feng, Liuyun Chong, Shufang Du, Yajian Duan, Ying Wang, Jiaxing Wang, Song Chen, and Tiangeng He. "Decreased Ratio of VEGF165b/VEGF in Aqueous Humor Predicts Progression of Diabetic Retinopathy." Ophthalmic Research 63, no. 6 (2020): 517–23. http://dx.doi.org/10.1159/000508250.

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<b><i>Background:</i></b> Different splicing of vascular endothelial growth factor (VEGF) gene results in 2 families of VEGF, the proangiogenic isoforms (VEGF<sub>xxx</sub>a) and the antiangiogenic isoforms (VEGF<sub>xxx</sub>b). VEGF<sub>165</sub>b is the major antiangiogenic isoform of VEGF and the most studied member of the VEGF<sub>xxx</sub>b family so far. <b><i>Objectives:</i></b> To determine the concentration of VEGF<sub>165</sub>b and VEGF in the aqueous humor (AH) in diabetic eyes with or without diabetic retinopathy (DR) and to address the predictive value of VEGF<sub>165</sub>b/VEGF ratio for progression of DR. <b><i>Methods:</i></b> AH samples from 20 eyes in healthy controls (CON group), 40 eyes in diabetic patients without DR (nDR group), and 30 eyes in diabetic patients with mild nonproliferative DR (DR group) were collected. All of the patients were followed up for at least 5 years. VEGF<sub>165</sub>b and VEGF levels of AH samples were measured by enzyme-linked immunosorbent assay (ELISA). The predictive value of the initial VEGF<sub>165</sub>b/VEGF ratio for progression of DR was studied. <b><i>Results:</i></b> The mean concentration of VEGF<sub>165</sub>b significantly decreased in diabetic eyes vs. controls. The mean concentration of VEGF significantly increased in the DR group vs. the CON group. The VEGF<sub>165</sub>b/VEGF ratio was significantly lower in diabetic patients compared to the CON group. The VEGF<sub>165</sub>b/VEGF ratio was significantly lower in diabetic patients compared to the control group. The mean follow-up was 66.1months (range 60–71 months). The risk of DR progression was greater with a lower VEGF<sub>165</sub>b/VEGF ratio. <b><i>Conclusion:</i></b> The VEGF<sub>165</sub>b/VEGF ratio is lower in the AH of DR patients and the decreased ratio of VEGF<sub>165</sub>b/VEGF predicts DR progression.

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Bills, VL, DO Bates, PW Soothill, and T. Overton. "PM.22 The Role of VEGF165B in Trophoblast Survival – Implications For Pre-Eclampsia Pathophysiology." Archives of Disease in Childhood - Fetal and Neonatal Edition 98, Suppl 1 (April 2013): A31.3—A32. http://dx.doi.org/10.1136/archdischild-2013-303966.106.

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Boudria, A., S. Gout, M. Keramidas, E. Brambilla, J. L. Coll, S. Gazzeri, and B. Eymin. "VEGF165b : un marqueur de réponse aux thérapies anti-angiogéniques dans les cancers du poumon ?" Revue des Maladies Respiratoires 31, no. 7 (September 2014): 657. http://dx.doi.org/10.1016/j.rmr.2014.04.030.

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Manetti, Mirko, Serena Guiducci, Lidia Ibba-Manneschi, and Marco Matucci-Cerinic. "Impaired Angiogenesis in Systemic Sclerosis: The Emerging Role of the Antiangiogenic VEGF165b Splice Variant." Trends in Cardiovascular Medicine 21, no. 7 (October 2011): 204–10. http://dx.doi.org/10.1016/j.tcm.2012.05.011.

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Chen, Jing, Zhenyu Li, Sheng Zhang, Ruiguang Zhang, Meera Dassarath, and Gang Wu. "Effects of exogenous VEGF165b on invasion and migration of human lung adenocarcinoma A549 cells." Journal of Huazhong University of Science and Technology [Medical Sciences] 31, no. 5 (October 2011): 619–24. http://dx.doi.org/10.1007/s11596-011-0571-4.

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38

Kurtagic, Elma, Mark P. Jedrychowski, and Matthew A. Nugent. "Neutrophil elastase cleaves VEGF to generate a VEGF fragment with altered activity." American Journal of Physiology-Lung Cellular and Molecular Physiology 296, no. 3 (March 2009): L534—L546. http://dx.doi.org/10.1152/ajplung.90505.2008.

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Excessive neutrophil elastase (NE) activity and altered vascular endothelial growth factor (VEGF) signaling have independently been implicated in the development and progression of pulmonary emphysema. In the present study, we investigated the potential link between NE and VEGF. We noted that VEGF165is a substrate for NE. Digestion of purified VEGF165with NE generated a partially degraded disulfide-linked fragment of VEGF. Mass spectrometric analysis revealed that NE likely cleaves VEGF165at both the NH2and COOH termini to produce VEGF fragment chains ∼5 kDa reduced in size. NE treatment of VEGF-laden endothelial cell cultures and smooth muscle cells endogenously expressing VEGF generated VEGF fragments similar to those observed with purified VEGF165. NE-generated VEGF fragment showed significantly reduced binding to VEGF receptor 2 and heparin yet retained the ability to bind to VEGF receptor 1. Interestingly, VEGF fragment showed altered signaling in pulmonary artery endothelial cells compared with intact VEGF165. Specifically, treatment with VEGF fragment did not activate extracellular-regulated kinases 1 and 2 (ERK1/2), yet resulted in enhanced activation of protein kinase B (Akt). Treatment of monocyte/macrophage RAW 264.7 cells with VEGF fragment, on the other hand, led to both Akt and ERK1/2 activation, increased VEGFR1 expression, and stimulated chemotaxis. These findings suggest that the tissue response to NE-mediated injury might involve the generation of diffusible VEGF fragments that stimulate inflammatory cell recruitment and activation via VEGF receptor 1.

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Qiu, Y., R. M. Perrin, J. Woolard, T. G. Cui, R. Mushens, S. J. Harper, and D. O. Bates. "PC34 ANTIBODIES SPECIFIC TO THE C TERMINUS OF VEGF165b, DETECT PROTEIN IN NORMAL HUMAN PLASMA." Microcirculation 11, no. 6 (September 2004): 550. http://dx.doi.org/10.1080/10739680490488733.

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Zhang, Huiyong, Wenjiao Xia, Chen Liang, Xiaoyin Wang, Lingtong Zhi, Changjiang Guo, Zhiyuan Niu, and Wuling Zhu. "VEGF165b and its mutant demonstrate immunomodulatory, not merely anti-angiogenic functions, in tumor-bearing mice." Molecular Immunology 122 (June 2020): 132–40. http://dx.doi.org/10.1016/j.molimm.2020.04.005.

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Zhu, Rui-Yu, Xin Xin, Hui-yun Dai, Qi Li, Jian-Yong Lei, Yun Chen, and Jian Jin. "Expression and purification of recombinant human serum albumin fusion protein with VEGF165b in Pichia pastoris." Protein Expression and Purification 85, no. 1 (September 2012): 32–37. http://dx.doi.org/10.1016/j.pep.2012.06.009.

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Ganta, Vijay Chaitanya, Min Choi, Anna Kutateladze, and Brian H. Annex. "VEGF165b Modulates Endothelial VEGFR1–STAT3 Signaling Pathway and Angiogenesis in Human and Experimental Peripheral Arterial Disease." Circulation Research 120, no. 2 (January 20, 2017): 282–95. http://dx.doi.org/10.1161/circresaha.116.309516.

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Glass, C. A., S. J. Harper, and D. O. Bates. "The anti-angiogenic VEGF isoform VEGF165b transiently increases hydraulic conductivity, probably through VEGF receptor 1in vivo." Journal of Physiology 572, no. 1 (March 28, 2006): 243–57. http://dx.doi.org/10.1113/jphysiol.2005.103127.

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Zhang, Huiyong, Enchao Jia, Wenjiao Xia, Chengui Lu, and Wuling Zhu. "VEGF165b mutant with a prolonged half-life and enhanced anti-tumor potency in a mouse model." Journal of Biotechnology 284 (October 2018): 84–90. http://dx.doi.org/10.1016/j.jbiotec.2018.08.002.

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Fantin, Alessandro, Anastasia Lampropoulou, Valentina Senatore, James T. Brash, Claudia Prahst, Clemens A. Lange, Sidath E. Liyanage, et al. "VEGF165-induced vascular permeability requires NRP1 for ABL-mediated SRC family kinase activation." Journal of Experimental Medicine 214, no. 4 (March 13, 2017): 1049–64. http://dx.doi.org/10.1084/jem.20160311.

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The vascular endothelial growth factor (VEGF) isoform VEGF165 stimulates vascular growth and hyperpermeability. Whereas blood vessel growth is essential to sustain organ health, chronic hyperpermeability causes damaging tissue edema. By combining in vivo and tissue culture models, we show here that VEGF165-induced vascular leakage requires both VEGFR2 and NRP1, including the VEGF164-binding site of NRP1 and the NRP1 cytoplasmic domain (NCD), but not the known NCD interactor GIPC1. In the VEGF165-bound receptor complex, the NCD promotes ABL kinase activation, which in turn is required to activate VEGFR2-recruited SRC family kinases (SFKs). These results elucidate the receptor complex and signaling hierarchy of downstream kinases that transduce the permeability response to VEGF165. In a mouse model with choroidal neovascularisation akin to age-related macular degeneration, NCD loss attenuated vessel leakage without affecting neovascularisation. These findings raise the possibility that targeting NRP1 or its NCD interactors may be a useful therapeutic strategy in neovascular disease to reduce VEGF165-induced edema without compromising vessel growth.

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Stepan, Holger. "Angiogenic factors and pre-eclampsia: an early marker is needed." Clinical Science 116, no. 3 (January 8, 2009): 231–32. http://dx.doi.org/10.1042/cs20080598.

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Pre-eclampsia, a pregnancy complication characterized by hypertension and proteinuria, is still a major cause of neonatal and maternal mortality, and acute and long-term morbidities for both mother and neonate. There is mounting evidence that an imbalance between angiogenic factors, such as VEGF (vascular endothelial growth factor) or PlGF (placental growth factor), and factors inhibiting angiogenesis, such as sFlt1 (soluble fms-like tyrosine kinase 1) and sEng (soluble endoglin), are closely related to the pathogenesis of pre-eclampsia. In the present issue of Clinical Science, Bills and co-workers report that VEGF165b, an alternative splice variant of the VEGF pre-mRNA, is up-regulated in women with normal pregnancy and that this increase was delayed or diminished in women who developed pre-eclampsia. Thus this protein could serve (alone or in combination with other parameters) as a new marker for risk assessment in terms of pre-eclampsia.

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Bills, V. L., J. Varet, A. Millar, S. J. Harper, P. W. Soothill, and D. O. Bates. "Failure to up-regulate VEGF165b in maternal plasma is a first trimester predictive marker for pre-eclampsia." Clinical Science 116, no. 12 (May 14, 2009): 873. http://dx.doi.org/10.1042/cs1160873.

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Ehlken, Christoph, Emma S. Rennel, Daniel Michels, Bastian Grundel, Amelie Pielen, Bernd Junker, Andreas Stahl, et al. "Levels of VEGF but not VEGF165b are Increased in the Vitreous of Patients With Retinal Vein Occlusion." American Journal of Ophthalmology 152, no. 2 (August 2011): 298–303. http://dx.doi.org/10.1016/j.ajo.2011.01.040.

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Cunningham, Sonia A., Tuan M. Tran, M. Pia Arrate, Robert Bjercke, and Tommy A. Brock. "KDR activation is crucial for VEGF165-mediated Ca2+mobilization in human umbilical vein endothelial cells." American Journal of Physiology-Cell Physiology 276, no. 1 (January 1, 1999): C176—C181. http://dx.doi.org/10.1152/ajpcell.1999.276.1.c176.

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We have prepared a polyclonal mouse antibody directed against the first three immunoglobulin-like domains of the kinase insert domain-containing receptor (KDR) tyrosine kinase. It possesses the ability to inhibit binding of the 165-amino acid splice variant of vascular endothelial cell growth factor (VEGF165) to recombinant KDR in vitro as well as to reduce VEGF165binding to human umbilical vein endothelial cells (HUVEC). These results confirm that the first three immunoglobulin-like domains of KDR are involved in VEGF165interactions. The anti-KDR antibody is able to completely block VEGF165-mediated intracellular Ca2+mobilization in HUVEC. Therefore, it appears that binding of VEGF165to the fms-like tyrosine kinase (Flt-1) in these cells does not translate into a Ca2+response. This is further exemplified by the lack of response to placental growth factor (PlGF), an Flt-1-specific ligand. Additionally, PlGF is unable to potentiate the effects of submaximal concentrations of VEGF165. Surprisingly, the VEGF-PlGF heterodimer was also very inefficient at eliciting a Ca2+signaling event in HUVEC. We conclude that KDR activation is crucial for mobilization of intracellular Ca2+in HUVEC in response to VEGF165.

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Adefolaju, Gbenga Anthony, Kathrine Elizabeth Scholtz, and Margot Jill Hosie. "Antiangiogenic VEGF165b Expression in Human Breast MCF-7 and MCF-10A Cells Exposed to Reverse Transcriptase and Protease Inhibitors." International Journal of Morphology 35, no. 1 (March 2017): 148–56. http://dx.doi.org/10.4067/s0717-95022017000100024.

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