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Articoli di riviste sul tema "Vascular endothelial growth factor-receptor 2"

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Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 20 febbraio 2023

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1

Jackson, Tanisha A., Harry E. Taylor, Deva Sharma, Stephen Desiderio e Sonye K. Danoff. "Vascular Endothelial Growth Factor Receptor-2". Journal of Biological Chemistry 280, n. 33 (7 giugno 2005): 29856–63. http://dx.doi.org/10.1074/jbc.m500335200.

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2

Zhao, B., G. Smith, J. Cai, A. Ma e M. Boulton. "Vascular endothelial growth factor C promotes survival of retinal vascular endothelial cells via vascular endothelial growth factor receptor-2". British Journal of Ophthalmology 91, n. 4 (30 agosto 2006): 538–45. http://dx.doi.org/10.1136/bjo.2006.101543.

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3

Hu, Xue-Ming, Wei Yang, Li-Xia Du, Wen-Qiang Cui, Wen-Li Mi, Qi-Liang Mao-Ying, Yu-Xia Chu e Yan-Qing Wang. "Vascular Endothelial Growth Factor A Signaling Promotes Spinal Central Sensitization and Pain-related Behaviors in Female Rats with Bone Cancer". Anesthesiology 131, n. 5 (1 novembre 2019): 1125–47. http://dx.doi.org/10.1097/aln.0000000000002916.

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Abstract Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New Background Cancer pain is a pervasive clinical symptom impairing life quality. Vascular endothelial growth factor A has been well studied in tumor angiogenesis and is recognized as a therapeutic target for anti-cancer treatment. This study tested the hypothesis that vascular endothelial growth factor A and vascular endothelial growth factor receptor 2 contribute to bone cancer pain regulation associated with spinal central sensitization. Methods This study was performed on female rats using a metastatic breast cancer bone pain model. Nociceptive behaviors were evaluated by mechanical allodynia, thermal hyperalgesia, spontaneous pain, and CatWalk gait analysis. Expression levels were measured by real-time quantitative polymerase chain reaction, western blot, and immunofluorescence analysis. Excitatory synaptic transmission was detected by whole-cell patch-clamp recordings. The primary outcome was the effect of pharmacologic intervention of spinal vascular endothelial growth factor A/vascular endothelial growth factor receptor 2–signaling on bone cancer pain behaviors. Results The mRNA and protein expression of vascular endothelial growth factor A and vascular endothelial growth factor receptor 2 were upregulated in tumor-bearing rats. Spinal blocking vascular endothelial growth factor A or vascular endothelial growth factor receptor 2 significantly attenuated tumor-induced mechanical allodynia (mean ± SD: vascular endothelial growth factor A, 7.6 ± 2.6 g vs. 5.3 ± 3.3 g; vascular endothelial growth factor receptor 2, 7.8 ± 3.0 g vs. 5.2 ± 3.4 g; n = 6; P < 0.0001) and thermal hyperalgesia (mean ± SD: vascular endothelial growth factor A, 9.0 ± 2.4 s vs. 7.4 ± 2.7 s; vascular endothelial growth factor receptor 2, 9.3 ± 2.5 s vs. 7.5 ± 3.1 s; n = 6; P < 0.0001), as well as spontaneous pain and abnormal gaits. Exogenous vascular endothelial growth factor A enhanced excitatory synaptic transmission in a vascular endothelial growth factor receptor 2–dependent manner, and spinal injection of exogenous vascular endothelial growth factor A was sufficient to cause pain hypersensitivity via vascular endothelial growth factor receptor 2–mediated activation of protein kinase C and Src family kinase in naïve rats. Moreover, spinal blocking vascular endothelial growth factor A/vascular endothelial growth factor receptor 2 pathways suppressed protein kinase C-mediated N-methyl-d-aspartate receptor activation and Src family kinase-mediated proinflammatory cytokine production. Conclusions Vascular endothelial growth factor A/vascular endothelial growth factor receptor 2 contributes to central sensitization and bone cancer pain via activation of neuronal protein kinase C and microglial Src family kinase pathways in the spinal cord.
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Nico, Beatrice, Patrizia Corsi, Angelo Vacca, Luisa Roncali e Domenico Ribatti. "Vascular endothelial growth factor and vascular endothelial growth factor receptor-2 expression in mdx mouse brain". Brain Research 953, n. 1-2 (ottobre 2002): 12–16. http://dx.doi.org/10.1016/s0006-8993(02)03219-5.

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5

Ding, Yangyang, Kai Liu, Xinyu Zhao, Yingtao Lv, Rilei Yu e Congmin Kang. "Design, synthesis, and antitumor activity of novel benzoheterocycle derivatives as inhibitors of vascular endothelial growth factor receptor-2 tyrosine kinase". Journal of Chemical Research 44, n. 5-6 (20 gennaio 2020): 286–94. http://dx.doi.org/10.1177/1747519819899067.

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The vascular endothelial growth factor receptor-2 signaling pathway promotes the formation of new blood vessels, and vascular endothelial growth factor receptor-2 tyrosine kinase exists in both active and inactive conformations. Novel indole–benzimidazole and indole–benzothiazole derivatives joined by different linkers are designed and synthesized as inhibitors of vascular endothelial growth factor receptor-2 tyrosine kinase. All the synthesized compounds were evaluated for their cytotoxicity against four human cancer cell lines (HeLa, HT29, A549, and MDA-MB-435) and human umbilical vein endothelial cell. Meanwhile, the inhibitory activities against vascular endothelial growth factor receptor-2 are estimated in vitro and the binding interactions with dual conformations of vascular endothelial growth factor receptor-2 tyrosine kinase are evaluated by molecular docking. Compounds 5a–c and 14 show inhibitory activity against vascular endothelial growth factor receptor-2 tyrosine kinase and promising cytotoxicity, specifically with IC50 values ranging between 0.1 and 1 μM, which imply broad-spectrum antitumor activity. These results provide a deep insight into potential structural modifications for developing potent vascular endothelial growth factor receptor-2 tyrosine kinase inhibitors.
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6

Guo, Shanchun, Laronna S. Colbert, Miles Fuller, Yuanyuan Zhang e Ruben R. Gonzalez-Perez. "Vascular endothelial growth factor receptor-2 in breast cancer". Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1806, n. 1 (agosto 2010): 108–21. http://dx.doi.org/10.1016/j.bbcan.2010.04.004.

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7

Sallmon, Hannes, Sandra Akanbi, Sven C. Weber, Alexander Gratopp, Cornelia Rheinländer e Petra Koehne. "Ibuprofen and indomethacin differentially regulate vascular endothelial growth factor and its receptors in ductus arteriosus endothelial cells". Cardiology in the Young 28, n. 3 (4 dicembre 2017): 432–37. http://dx.doi.org/10.1017/s1047951117002311.

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AbstractBackgroundCyclooxygenase inhibitors are widely applied to facilitate ductal closure in preterm infants. The mechanisms that lead to patent ductus arteriosus closure are incompletely understood. Vascular endothelial growth factor plays pivotal roles during ductal closure and remodelling.AimThe aim of this study was to investigate the effects of ibuprofen and indomethacin on the expression of vascular endothelial growth factor and its receptors in a primary rat ductus arteriosus endothelial cell culture.MethodsProtein expression of vascular endothelial growth factor and vascular endothelial growth factor receptor 1 and 2 was confirmed in rat ductus arteriosus and aorta by immunofluorescence staining. Fetal rat endothelial cells were isolated from ductus arteriosus and aorta using immunomagnetic cell sorting and treated with ibuprofen or indomethacin. mRNA expression levels were assessed by quantitative polymerase chain reaction analysis.ResultsIn ductal endothelial cells, ibuprofen significantly induced vascular endothelial growth factor and its receptor 2, but not receptor 1, whereas indomethacin did not alter the expression levels of the vascular endothelial growth factor system. In contrast, ibuprofen significantly induced vascular endothelial growth factor and its receptors 1 and 2 in aortic endothelial cells, whereas indomethacin only induced vascular endothelial growth factor receptor 2.ConclusionOur results indicate differential effects of ibuprofen and indomethacin on the expression levels of the vascular endothelial growth factor system in ductus arteriosus endothelial cells. In addition, vessel-specific differences between ductal and aortic endothelial cells were found. Further in vivo studies are needed to elucidate the biological significance of these findings.
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Janvier, Annie, Sophie Nadeau, Johanne Baribeau e Thérèse Perreault. "Role of vascular endothelial growth factor receptor 1 and vascular endothelial growth factor receptor 2 in the vasodilator response to vascular endothelial growth factor in the neonatal piglet lung". Critical Care Medicine 33, n. 4 (aprile 2005): 860–66. http://dx.doi.org/10.1097/01.ccm.0000159563.97092.a7.

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Pedersen, H. G., J. Greenaway, T. Greve e J. Petrik. "248EXPRESSION AND LOCALIZATION OF VASCULAR ENDOTHELIAL GROWTH FACTOR AND VASCULAR ENDOTHELIAL GROWTH FACTOR RECEPTOR 2 IN EQUINE FOLLICLES". Reproduction, Fertility and Development 16, n. 2 (2004): 244. http://dx.doi.org/10.1071/rdv16n1ab248.

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Ovarian follicles undergo pronounced morphological changes, alternating between periods of growth and regression. The equine follicle will grow to an average of 45mm in diameter at ovulation, and during the phase of growth, there is an increase in blood supply to the follicle. Vascular endothelial growth factor (VEGF) is a cytokine that interacts with tyrosine kinase receptors to stimulate angiogenesis, endothelial cell proliferation and vascular permeability. The aim of the study was to evaluate the expression and localization of VEGF and the VEGF-receptor 2 (VEGF-R2) in equine follicles. Ovaries were collected from a slaughterhouse. Granulosa cells from follicles were pooled regardless of the size of the follicles. Western blots were performed using protein extracted from granulosa cells and follicular fluid. Blots were probed with rabbit anti-human VEGF and rabbit anti-mouse VEGF-R2 antibodies and visualized with chemiluminescence. Total RNA was extracted from granulosa cells and integrity of the RNA samples was tested by the amplification of β-actin. Complementary DNA was synthesized by reverse transcription, followed by polymerase chain reaction amplification of cDNA encoding with bovine primer sequences for VEGF and VEGF-R2. The PCR product was resolved on 1% agarose gel and the resulting VEGF and VEGF-R2 bands were sequenced. Immunostaining for VEGF and VEGF-R2 was performed on fixed, paraffin-embedded sections of follicle wall from follicles larger than 30mm. Western blot analysis of granulosa cell lysates revealed 22kDa bands for VEGF, and 210kDa bands for VEGF-R2. VEGF protein was present in follicular fluid, whereas VEGF-R2 was not detectable. RT-PCR experiments revealed the presence of VEGF and VEGF-R2 mRNA in isolated granulosa cells. Sequencing demonstrated 93% and 99% homology to known sequences of equine VEGF and VEGF-R2, respectively. Immunofluorescence experiments performed on dissected equine follicles localized VEGF to the granulosa cell layer and sporadically to the theca cell layer. VEGF-R2 co-localized with VEGF in the granulosa cells, and was relatively absent in the theca layer. The present study detected novel expression patterns for VEGF and VEGF-R2 in equine ovarian follicles. The results of these experiments suggest an extra-vascular role for the VEGF family in follicle development. Future studies will be directed at studying the genomic and proteonomic profiles of follicles during the selection of the dominant follicle in mares.
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Mandriota, Stefano J., Pierre-Alain Menoud e Michael S. Pepper. "Transforming Growth Factor 1 Down-regulates Vascular Endothelial Growth Factor Receptor 2/flk-1Expression in Vascular Endothelial Cells". Journal of Biological Chemistry 271, n. 19 (10 maggio 1996): 11500–11505. http://dx.doi.org/10.1074/jbc.271.19.11500.

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11

Nico, Beatrice, Domenica Mangieri, Patrizia Corsi, Michela De Giorgis, Angelo Vacca, Luisa Roncali e Domenico Ribatti. "Vascular endothelial growth factor-A, vascular endothelial growth factor receptor-2 and angiopoietin-2 expression in the mouse choroid plexuses". Brain Research 1013, n. 2 (luglio 2004): 256–59. http://dx.doi.org/10.1016/j.brainres.2004.04.016.

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KASAHARA, YASUNORI, RUBIN M TUDER, CARLYNE D COOL, DAVID A LYNCH, SONIA C FLORES e NORBERT F VOELKEL. "Endothelial Cell Death and Decreased Expression of Vascular Endothelial Growth Factor and Vascular Endothelial Growth Factor Receptor 2 in Emphysema". American Journal of Respiratory and Critical Care Medicine 163, n. 3 (marzo 2001): 737–44. http://dx.doi.org/10.1164/ajrccm.163.3.2002117.

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Elkar, Buğra, Mustafa Barış, Meryem Çalışır, Yasemin Çakır, Safiye Aktaş, Merve Tütüncü, M. Kürşat Şimşek, Mustafa Seçil, Osman Yılmaz e Zekiye Altun. "Endothelial Dysfunction in Breast Cancer In-Vivo Model". Proceedings 2, n. 25 (6 dicembre 2018): 1536. http://dx.doi.org/10.3390/proceedings2251536.

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Abstract (sommario):
Although the endothelial dysfunction is related with tumor development, there is no consensus on the suppressive or supportive effect on tumor growth. The goal of the present study was to evaluate endothelial dysfunction related factors in animal breast cancer model that was developed by administrating endothelial nitric oxide synthase blocking agent, Nitro-L-arginine methyl ester hydrochloride (L-NAME). Endothelial dysfunction related main factors such as nitric oxide synthase, interleukin-6, vascular endothelial growth factor receptor-2 and vascular endothelial cadherin were investigated by immunohistochemically in tumor and carotid artery tissues. In tumor tissues apoptosis was determined by TUNEL assay. The level of endothelin-1 in blood was measured by ELISA. İntima-media thickness of carotid artery was evaluated with Doppler-USG measurements. As a result, in this study it was shown that vascular endothelial growth factor receptor-2, endothelin-1, endothelial nitric oxide synthase, interleukin-6, vascular endothelial cadherin and E-selectin molecules play a role in reducing breast tumor growth based on endothelial dysfunction.
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14

Ho, Vivienne C., Li-Juan Duan, Chunxia Cronin, Bruce T. Liang e Guo-Hua Fong. "Elevated Vascular Endothelial Growth Factor Receptor-2 Abundance Contributes to Increased Angiogenesis in Vascular Endothelial Growth Factor Receptor-1–Deficient Mice". Circulation 126, n. 6 (7 agosto 2012): 741–52. http://dx.doi.org/10.1161/circulationaha.112.091603.

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15

Leblanc, Michelle E., Kahira L. Saez‐Torres, Issahy Cano, Zhengping Hu, Magali Saint‐Geniez, Yin‐Shan Ng e Patricia A. D'Amore. "Glycocalyx regulation of vascular endothelial growth factor receptor 2 activity". FASEB Journal 33, n. 8 (29 maggio 2019): 9362–73. http://dx.doi.org/10.1096/fj.201900011r.

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Zecchin, Annalisa, Lucia Pattarini, Maria Ines Gutierrez, Miguel Mano, Antonello Mai, Sergio Valente, Mike P. Myers, Sergio Pantano e Mauro Giacca. "Reversible acetylation regulates vascular endothelial growth factor receptor-2 activity". Journal of Molecular Cell Biology 6, n. 2 (11 marzo 2014): 116–27. http://dx.doi.org/10.1093/jmcb/mju010.

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Papakyriakou, Athanasios, Maria E Katsarou, Maria Belimezi, Michael Karpusas e Dionisios Vourloumis. "Discovery of Potent Vascular Endothelial Growth Factor Receptor-2 Inhibitors". ChemMedChem 5, n. 1 (4 gennaio 2010): 118–29. http://dx.doi.org/10.1002/cmdc.200900373.

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Pavlov, K. A., E. S. Gershtein, E. A. Dubova e A. I. Shchegolev. "Vascular Endothelial Growth Factor and Type 2 Receptor for This Factor in Vascular Malformations". Bulletin of Experimental Biology and Medicine 150, n. 4 (febbraio 2011): 481–84. http://dx.doi.org/10.1007/s10517-011-1174-6.

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19

Qin, Jun, Xinpu Chen, Li-yuan Yu-Lee, Ming-Jer Tsai e Sophia Y. Tsai. "Nuclear Receptor COUP-TFII Controls Pancreatic Islet Tumor Angiogenesis by Regulating Vascular Endothelial Growth Factor/Vascular Endothelial Growth Factor Receptor-2 Signaling". Cancer Research 70, n. 21 (26 ottobre 2010): 8812–21. http://dx.doi.org/10.1158/0008-5472.can-10-0551.

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Dunk, Caroline, e Asif Ahmed. "Vascular Endothelial Growth Factor Receptor-2-Mediated Mitogenesis Is Negatively Regulated by Vascular Endothelial Growth Factor Receptor-1 in Tumor Epithelial Cells". American Journal of Pathology 158, n. 1 (gennaio 2001): 265–73. http://dx.doi.org/10.1016/s0002-9440(10)63965-x.

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Pepper, Michael S., e Stefano J. Mandriota. "Regulation of Vascular Endothelial Growth Factor Receptor-2 (Flk-1) Expression in Vascular Endothelial Cells". Experimental Cell Research 241, n. 2 (giugno 1998): 414–25. http://dx.doi.org/10.1006/excr.1998.4072.

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Yang, Suya, Xiaohua Xin, Constance Zlot, Gladys Ingle, Germaine Fuh, Bing Li, Barbara Moffat, Abraham M. de Vos e Mary E. Gerritsen. "Vascular Endothelial Cell Growth Factor-Driven Endothelial Tube Formation Is Mediated by Vascular Endothelial Cell Growth Factor Receptor-2, a Kinase Insert Domain-Containing Receptor". Arteriosclerosis, Thrombosis, and Vascular Biology 21, n. 12 (dicembre 2001): 1934–40. http://dx.doi.org/10.1161/hq1201.099432.

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Stoletov, Konstantin V., Kirsty E. Ratcliffe e Bruce I. Terman. "Fibroblast growth factor receptor substrate 2 participates in vascular endothelial growth factor‐induced signaling". FASEB Journal 16, n. 10 (21 giugno 2002): 1283–85. http://dx.doi.org/10.1096/fj.01-0835fje.

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Janer, J., S. Andersson, C. Haglund, R. Karikoski e P. Lassus. "Placental Growth Factor and Vascular Endothelial Growth Factor Receptor-2 in Human Lung Development". PEDIATRICS 122, n. 2 (1 agosto 2008): 340–46. http://dx.doi.org/10.1542/peds.2007-1941.

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Soriano, Jesus V., Ningfei Liu, Yang Gao, Zhu-Jun Yao, Toshio Ishibashi, Charles Underhill, Terrence R. Burke e Donald P. Bottaro. "Inhibition of angiogenesis by growth factor receptor bound protein 2-Src homology 2 domain bound antagonists". Molecular Cancer Therapeutics 3, n. 10 (1 ottobre 2004): 1289–99. http://dx.doi.org/10.1158/1535-7163.1289.3.10.

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Abstract (sommario):
Abstract Growth factor receptor bound protein 2 (Grb2) is an intracellular adaptor protein that participates in the signal transduction cascades of several angiogenic factors, including hepatocyte growth factor, basic fibroblast growth factor, and vascular endothelial growth factor. We described previously the potent blockade of hepatocyte growth factor–stimulated cell motility, matrix invasion, and epithelial tubulogenesis by synthetic Grb2-Src homology 2 (SH2) domain binding antagonists. Here, we show that these binding antagonists block basic morphogenetic events required for angiogenesis, including hepatocyte growth factor–, vascular endothelial growth factor–, and basic fibroblast growth factor–stimulated endothelial cell proliferation and migration, as well as phorbol 12-myristate 13-acetate–stimulated endothelial cell migration and matrix invasion. The Grb2-SH2 domain binding antagonists also impair angiogenesis in vitro, as shown by the inhibition of cord formation by macrovascular endothelial cells on Matrigel. We further show that a representative compound inhibits angiogenesis in vivo as measured using a chick chorioallantoic membrane assay. These results suggest that Grb2 is an important mediator of key proangiogenic events, with potential application to pathologic conditions where neovascularization contributes to disease progression. In particular, the well-characterized role of Grb2 in signaling cell cycle progression together with our present findings suggests that Grb2-SH2 domain binding antagonists have the potential to act as anticancer drugs that target both tumor and vascular cell compartments.
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Kyzas, Panayiotis A., Dimitrios Stefanou, Anna Batistatou e Niki J. Agnantis. "Potential autocrine function of vascular endothelial growth factor in head and neck cancer via vascular endothelial growth factor receptor-2". Modern Pathology 18, n. 4 (8 ottobre 2004): 485–94. http://dx.doi.org/10.1038/modpathol.3800295.

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Furuta, Takahisa, Mikio Kimura e Naohiro Watanabe. "Elevated Levels of Vascular Endothelial Growth Factor (VEGF) and Soluble Vascular Endothelial Growth Factor Receptor (VEGFR)-2 in Human Malaria". American Journal of Tropical Medicine and Hygiene 82, n. 1 (1 gennaio 2010): 136–39. http://dx.doi.org/10.4269/ajtmh.2010.09-0203.

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Sawada, Mayumi, Tetsuro Oishi, Hiroaki Komatsu, Shinya Sato, Jun Chikumi, Michiko Nonaka, Akiko Kudoh, Daiken Osaku e Tasuku Harada. "Serum vascular endothelial growth factor A and vascular endothelial growth factor receptor 2 as prognostic biomarkers for uterine cervical cancer". International Journal of Clinical Oncology 24, n. 12 (24 giugno 2019): 1612–19. http://dx.doi.org/10.1007/s10147-019-01495-x.

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Odorisio, Teresa, Cataldo Schietroma, M. Letizia Zaccaria, Francesca Cianfarani, Cecilia Tiveron, Laura Tatangelo, Cristina M. Failla e Giovanna Zambruno. "Mice overexpressing placenta growth factor exhibit increased vascularization and vessel permeability". Journal of Cell Science 115, n. 12 (15 giugno 2002): 2559–67. http://dx.doi.org/10.1242/jcs.115.12.2559.

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Abstract (sommario):
Placenta growth factor (PlGF) is a member of the vascular endothelial growth factor (VEGF) family, comprising at least five cytokines specifically involved in the regulation of vascular and/or lymphatic endothelium differentiation. Several lines of evidence indicate a role for PlGF in monocyte chemotaxis and in potentiating the activity of VEGF, but the exact function of this cytokine is not fully understood. To define the biological role of PlGF in vivo, we have produced a transgenic mouse model overexpressing this factor in the skin by using a keratin 14 promoter cassette. Our data indicate that PlGF has strong angiogenic properties in both fetal and adult life. PlGF overexpression results in a substantial increase in the number,branching and size of dermal blood vessels as well as in enhanced vascular permeability. Indeed, intradermally injected recombinant PlGF was able to induce vessel permeability in wild-type mice. The analysis of vascular endothelial growth factor receptor 1/flt-1 and vascular endothelial growth factor receptor 2/flk-1 indicates that the two receptors are induced in the skin endothelium of transgenic mice suggesting that both are involved in mediating the effect of overexpressed PlGF.
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Leonard, F., I. Ernens, M. Vausort, E. Velot, M. Rolland-Turner, T. Chan, Z. Lu et al. "D003 Angiogenic effects of adenosine involve regulation of vascular endothelial growth factor and soluble vascular endothelial growth factor receptor -1". Archives of Cardiovascular Diseases 102 (marzo 2009): S36—S37. http://dx.doi.org/10.1016/s1875-2136(09)72213-2.

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Chung, Tae-Wook, Eun-Yeong Kim, Hee-Jung Choi, Chang Woo Han, Se Bok Jang, Keuk-Jun Kim, Ling Jin, Young Jun Koh e Ki-Tae Ha. "6′-Sialylgalactose inhibits vascular endothelial growth factor receptor 2-mediated angiogenesis". Experimental & Molecular Medicine 51, n. 10 (ottobre 2019): 1–13. http://dx.doi.org/10.1038/s12276-019-0311-6.

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Abstract Angiogenesis should be precisely regulated because disordered neovascularization is involved in the aggravation of multiple diseases. The vascular endothelial growth factor (VEGF)-A/VEGF receptor 2 (VEGFR-2) axis is crucial for controlling angiogenic responses in vascular endothelial cells (ECs). Therefore, inactivating VEGFR-2 signaling may effectively suppress aberrant angiogenesis and alleviate related symptoms. In this study, we performed virtual screening, identified the synthetic disaccharide 6′-sialylgalactose (6SG) as a potent VEGFR-2-binding compound and verified its high binding affinity by Biacore assay. 6SG effectively suppressed VEGF-A-induced VEGFR-2 phosphorylation and subsequent in vitro angiogenesis in HUVECs without inducing cytotoxicity. 6SG also inhibited VEGF-A-induced extracellular-regulated kinase (ERK)/Akt activation and actin stress fiber formation in HUVECs. We demonstrated that 6SG inhibited retinal angiogenesis in a mouse model of retinopathy of prematurity and tumor angiogenesis in a xenograft mouse model. Our results suggest a potential therapeutic benefit of 6SG in inhibiting angiogenesis in proangiogenic diseases, such as retinopathy and cancer.
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Claesson-Welsh, L. "Signal transduction by vascular endothelial growth factor receptors". Biochemical Society Transactions 31, n. 1 (1 febbraio 2003): 20–24. http://dx.doi.org/10.1042/bst0310020.

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Abstract (sommario):
Vascular endothelial growth factor (VEGF)/vascular permeability factor is the prototype for a growing family of dimeric growth factors, which exert their effects on vascular and lymphatic endothelial cells, as well as on a wide range of other cell types. Gene targeting shows that most, if not all, of the factors and receptors in this family serve critical functions during vascular development or in adult physiological and pathological angiogenesis. Growing tumours produce VEGF, and many different strategies for inhibiting tumour growth by inhibiting VEGF production are being tested in clinical trials at present. This review focuses on the signal transduction properties of VEGF receptor-1 and VEGF receptor-2.
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Knod, Leslie, Eileen C. Donovan, Artur Chernoguz, Kelly M. Crawford, Mary R. Dusing e Jason S. Frischer. "Vascular endothelial growth factor receptor-2 inhibition in experimental murine colitis". Journal of Surgical Research 184, n. 1 (settembre 2013): 101–7. http://dx.doi.org/10.1016/j.jss.2013.04.026.

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Lamy, Sylvie, Amira Ouanouki, Richard Béliveau e Richard R. Desrosiers. "Olive oil compounds inhibit vascular endothelial growth factor receptor-2 phosphorylation". Experimental Cell Research 322, n. 1 (marzo 2014): 89–98. http://dx.doi.org/10.1016/j.yexcr.2013.11.022.

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Bernatchez, Pascal N., Lisette Acevedo, Carlos Fernandez-Hernando, Takahisa Murata, Cecile Chalouni, Jiae Kim, Hediye Erdjument-Bromage et al. "Myoferlin Regulates Vascular Endothelial Growth Factor Receptor-2 Stability and Function". Journal of Biological Chemistry 282, n. 42 (16 agosto 2007): 30745–53. http://dx.doi.org/10.1074/jbc.m704798200.

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Murdaca, Joseph, Caroline Treins, Marie-Noëlle Monthouël-Kartmann, Rodolphe Pontier-Bres, Sharad Kumar, Emmanuel Van Obberghen e Sophie Giorgetti-Peraldi. "Grb10 Prevents Nedd4-mediated Vascular Endothelial Growth Factor Receptor-2 Degradation". Journal of Biological Chemistry 279, n. 25 (1 aprile 2004): 26754–61. http://dx.doi.org/10.1074/jbc.m311802200.

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Gluzman-Poltorak, Zoya, Tzafra Cohen, Masabumi Shibuya e Gera Neufeld. "Vascular Endothelial Growth Factor Receptor-1 and Neuropilin-2 Form Complexes". Journal of Biological Chemistry 276, n. 22 (14 marzo 2001): 18688–94. http://dx.doi.org/10.1074/jbc.m006909200.

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38

McGrath-Morrow, Sharon A., Cecilia Cho, Chung Cho, Lijie Zhen, Daniel J. Hicklin e Rubin M. Tuder. "Vascular Endothelial Growth Factor Receptor 2 Blockade Disrupts Postnatal Lung Development". American Journal of Respiratory Cell and Molecular Biology 32, n. 5 (maggio 2005): 420–27. http://dx.doi.org/10.1165/rcmb.2004-0287oc.

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39

Dimtsas, Georgios S., Eleni C. Georgiadi, Petros Karakitsos, Theodoros P. Vassilakopoulos, Irene Thymara, Penelope Korkolopoulou, Efstratios Patsouris, Christos Kittas e Ipatia A. Doussis-Anagnostopoulou. "Prognostic significance of immunohistochemical expression of the angiogenic molecules vascular endothelial growth factor-A, vascular endothelial growth factor receptor-1 and vascular endothelial growth factor receptor-2 in patients with classical Hodgkin lymphoma". Leukemia & Lymphoma 55, n. 3 (16 luglio 2013): 558–64. http://dx.doi.org/10.3109/10428194.2013.813629.

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40

Joukov, Vladimir, Vijay Kumar, Tarja Sorsa, Elena Arighi, Herbert Weich, Olli Saksela e Kari Alitalo. "A Recombinant Mutant Vascular Endothelial Growth Factor-C that Has Lost Vascular Endothelial Growth Factor Receptor-2 Binding, Activation, and Vascular Permeability Activities". Journal of Biological Chemistry 273, n. 12 (20 marzo 1998): 6599–602. http://dx.doi.org/10.1074/jbc.273.12.6599.

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41

Park, Hwan-Woo, Hyo-Jin Jeon e Mi-Sook Chang. "Vascular endothelial growth factor enhances axonal outgrowth in organotypic spinal cord slices via vascular endothelial growth factor receptor 1 and 2". Tissue Engineering and Regenerative Medicine 13, n. 5 (ottobre 2016): 601–9. http://dx.doi.org/10.1007/s13770-016-0051-9.

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42

Srabovic, Nahida, Zlata Mujagic, Jasminka Mujanovic-Mustedanagic, Adaleta Softic, Zdeno Muminovic, Adi Rifatbegovic e Lejla Begic. "Vascular Endothelial Growth Factor Receptor-1 Expression in Breast Cancer and Its Correlation to Vascular Endothelial Growth Factor A". International Journal of Breast Cancer 2013 (2013): 1–6. http://dx.doi.org/10.1155/2013/746749.

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Abstract (sommario):
VEGF-A is the most potent angiogenic factor in tumour angiogenesis. Its effects are mediated via two receptors VEGFR-1 and VEGFR-2. Primary aim of our study was to examine the expression of VEGFR-1 in breast cancer and its correlation to VEGF expression, lymph node status, tumour size, histological grade, and hormone receptor status. To examine the VEGFR-1 and VEGF expressions in tumour and surrounding tissue of 51 breast cancer patients, and in healthy breast tissue of 30 benign breast diseases patients, we used three-step immunohistochemical staining. VEGFR-1 and VEGF expressions were significantly increased in breast cancer tumour in relation to surrounding tissue (P<0.01), and the VEGF expression was significantly increased in lymph node positive breast cancer patients (P<0.01). VEGFR-1 and VEGF expressions were significantly higher in breast cancer tumour compared with healthy breast tissue (P<0.01). Significant correlation between VEGF and VEGFR-1 expressions was found (P<0.05). No significant correlations between VEGF and VEGFR-1 expressions and tumour size, histological grade, and hormone receptor status were found. Increased expression of VEGFR-1 and VEGF in breast cancer tumour and significant correlation between these proteins suggest the possible role of VEGF/VEGFR-1 signalization in breast cancer development, although VEGFR-1 potential prognostic value was not confirmed.
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43

Gallicchio, Margherita, Stefania Mitola, Donatella Valdembri, Roberto Fantozzi, Brian Varnum, Gian Carlo Avanzi e Federico Bussolino. "Inhibition of vascular endothelial growth factor receptor 2–mediated endothelial cell activation by Axl tyrosine kinase receptor". Blood 105, n. 5 (1 marzo 2005): 1970–76. http://dx.doi.org/10.1182/blood-2004-04-1469.

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AbstractGAS6, the product of a growth arrest specific (GAS) gene, is the ligand of the tyrosine kinase receptor Axl. GAS6 and Axl are both expressed in endothelial cells, where they are involved in many processes such as leukocyte transmigration through capillaries and neointima formation in injured vessels. Here, we show that Axl stimulation by GAS6 results in inhibition of the ligand-dependent activation of vascular endothelial growth factor (VEGF) receptor 2 and the consequent activation of an angiogenic program in vascular endothelial cells. GAS6 inhibits chemotaxis of endothelial cells stimulated by VEGF-A isoforms, but not that triggered by fibroblast growth factor-2 or hepatocyte growth factor. Furthermore, it inhibits endothelial cell morphogenesis on Matrigel and VEGF-A–dependent vascularization of chick chorion allantoid membrane. GAS6 activates the tyrosine phosphatase SHP-2 (SH2 domain-containing tyrosine phosphatase 2), which is instrumental in the negative feedback exerted by Axl on VEGF-A activities. A dominant-negative SHP-2 mutant, in which Cys 459 is substituted by Ser, reverted the effect of GAS6 on stimulation of VEGF receptor 2 and endothelial chemotaxis triggered by VEGF-A. These studies provide the first demonstration of a cross talk between Axl and VEGF receptor 2 and add new information on the regulation of VEGF-A activities during tissue vascularization.
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44

Hewett, Peter W., Takeshi Fujisawa, Samir Sissaoui, Meng Cai, Geraldine Gueron, Bahjat Al-Ani, Melissa Cudmore et al. "Carbon monoxide inhibits sprouting angiogenesis and vascular endothelial growth factor receptor-2 phosphorylation". Thrombosis and Haemostasis 113, n. 02 (marzo 2015): 329–37. http://dx.doi.org/10.1160/th14-01-0002.

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SummaryCarbon monoxide (CO) is a gaseous autacoid known to positively regulate vascular tone; however, its role in angiogenesis is unknown. The aim of this study was to investigate the effect of CO on angiogenesis and vascular endothelial growth factor (VEGF) receptor-2 phosphorylation. Human umbilical vein endothelial cells (HUVECs) were cultured on growth factor-reduced Matrigel and treated with a CO-releasing molecule (CORM-2) or exposed to CO gas (250 ppm). Here, we report the surprising finding that exposure to CO inhibits vascular endothelial growth factor (VEGF)-induced endothelial cell actin reorganisation, cell proliferation, migration and capillary-like tube formation. Similarly, CO suppressed VEGF-mediated phosphorylation of VEGFR-2 at tyrosine residue 1175 and 1214 and basic fibroblast growth factor- (FGF-2) and VEGF-mediated Akt phosphorylation. Consistent with these data, mice exposed to 250 ppm CO (1h/day for 14 days) exhibited a marked decrease in FGF-2-induced Matrigel plug angiogenesis (p<0.05). These data establish a new biological function for CO in angiogenesis and point to a potential therapeutic use for CO as an anti-angiogenic agent in tumour suppression.
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45

Robillard, Stéphanie, Clément Mercier, Valérie Breton, Judith Paquin-Veillette, Andréanne Guay, Farah Lizotte e Pedro Geraldes. "Ablation of angiotensin type 2 receptor prevents endothelial nitric oxide synthase glutathionylation and nitration in ischaemic abductor muscle of diabetic mice". Diabetes and Vascular Disease Research 17, n. 1 (14 novembre 2019): 147916411988397. http://dx.doi.org/10.1177/1479164119883978.

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Peripheral artery disease is a severe complication of diabetes. We have reported that the deletion of angiotensin type 2 receptor in diabetic mice promoted vascular angiogenesis in the ischaemic muscle 4 weeks following ischaemia. However, the angiotensin type 2 receptor deletion beneficial effects occurred 2 weeks post surgery suggesting that angiotensin type 2 receptor may regulate other pro-angiogenic signalling pathways during the early phases of ischaemia. Nondiabetic and diabetic angiotensin type 2 receptor–deficient mice ( Agtr2−/Y) underwent femoral artery ligation after 2 months of diabetes. Blood perfusion was measured every week up to 2 weeks post surgery. Expression of vascular endothelial growth factor, vascular endothelial growth factor receptor and endothelial nitric oxide synthase expression and activity were evaluated. Blood flow reperfusion in the ischaemic muscle of diabetic Agtr2+/Y mice was recovered at 35% as compared to a 68% recovery in diabetic Agtr2−/Y mice. The expression of vascular endothelial growth factor and its receptors was diminished in diabetic Agtr2+/Y mice, an observation not seen in diabetic Agtr2−/Y mice. Interestingly, Agtr2−/Y mice were protected from diabetes-induced glutathionylation, nitration and decreased endothelial nitric oxide synthase expression, which correlated with reduced endothelial cell death and enhanced vascular density in diabetic ischaemic muscle. In conclusion, our results suggest that the deletion of angiotensin type 2 receptor promotes blood flow reperfusion in diabetes by favouring endothelial cell survival and function.
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46

Ebos, John M. L., Christina R. Lee, Elena Bogdanovic, Jennifer Alami, Paul Van Slyke, Giulio Francia, Ping Xu, Anthony J. Mutsaers, Daniel J. Dumont e Robert S. Kerbel. "Vascular Endothelial Growth Factor–Mediated Decrease in Plasma Soluble Vascular Endothelial Growth Factor Receptor-2 Levels as a Surrogate Biomarker for Tumor Growth". Cancer Research 68, n. 2 (15 gennaio 2008): 521–29. http://dx.doi.org/10.1158/0008-5472.can-07-3217.

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47

Wu, Jing, e Emery H. Bresnick. "Glucocorticoid and Growth Factor Synergism Requirement for Notch4 Chromatin Domain Activation". Molecular and Cellular Biology 27, n. 6 (12 gennaio 2007): 2411–22. http://dx.doi.org/10.1128/mcb.02152-06.

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Abstract (sommario):
ABSTRACT The Notch signaling pathway modulates cell fate in diverse contexts, including vascular development. Notch4 is selectively expressed in vascular endothelium and regulates vascular remodeling. The signal-dependent transcription factor activator protein 1 (AP-1) activates Notch4 transcription in endothelial cells, but other factors/signals that regulate Notch4 are largely unknown. We demonstrate that, unlike the established transrepression mechanism in which the glucocorticoid receptor (GR) antagonizes AP-1, AP-1 and GR synergistically activated Notch4 transcription in endothelial cells. Fibroblast growth factor 2 (FGF-2) and cortisol induced AP-1 and GR occupancy, respectively, at a Notch4 promoter composite response element consisting of an imperfect half-glucocorticoid response element and an AP-1 motif, which mediated signal-dependent activation. Analysis of Notch4 promoter complex assembly provided evidence that GR and AP-1 independently occupy the composite response element, but AP-1 stabilizes GR occupancy. In multipotent 10T1/2 cells, FGF-2 and cortisol induced a histone modification pattern at the Notch4 locus mimicking that present in endothelial cells and reprogrammed Notch4 from a repressed to an active state. These results establish the molecular basis for a novel AP-1/GR-Notch4 axis in vascular endothelium.
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48

Sert, Tuba, F. Yeşim Kırzıoğlu, Özlem Fentoğlu, Firdevs Aylak e Tamer Mungan. "Serum Placental Growth Factor, Vascular Endothelial Growth Factor, Soluble Vascular Endothelial Growth Factor Receptor-1 and -2 Levels in Periodontal Disease, and Adverse Pregnancy Outcomes". Journal of Periodontology 82, n. 12 (dicembre 2011): 1735–48. http://dx.doi.org/10.1902/jop.2011.100740.

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49

Wang, Yuchuan, Jinyong Lin, Luxia Chen, Liming Wang, Peng Hao, Ruifang Han, Ming Ying e Xuan Li. "Expression of Peroxiredoxin 2 and Vascular Endothelial Growth Factor Receptor 2 in Pterygium". Cornea 36, n. 7 (luglio 2017): 841–44. http://dx.doi.org/10.1097/ico.0000000000001213.

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50

Magnusson, P. "Deregulation of Flk-1/vascular endothelial growth factor receptor-2 in fibroblast growth factor receptor-1-deficient vascular stem cell development". Journal of Cell Science 117, n. 8 (15 marzo 2004): 1513–23. http://dx.doi.org/10.1242/jcs.00999.

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