Gotowe bibliografie tematyczne / Vascular endothelial growth factor-receptor 2

Gotowa bibliografia na temat „Vascular endothelial growth factor-receptor 2”

Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 20 lutego 2023

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Artykuły w czasopismach na temat "Vascular endothelial growth factor-receptor 2"

Jackson, Tanisha A., Harry E. Taylor, Deva Sharma, Stephen Desiderio i Sonye K. Danoff. "Vascular Endothelial Growth Factor Receptor-2". Journal of Biological Chemistry 280, nr 33 (7.06.2005): 29856–63. http://dx.doi.org/10.1074/jbc.m500335200.

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Zhao, B., G. Smith, J. Cai, A. Ma i 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, nr 4 (30.08.2006): 538–45. http://dx.doi.org/10.1136/bjo.2006.101543.

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Hu, Xue-Ming, Wei Yang, Li-Xia Du, Wen-Qiang Cui, Wen-Li Mi, Qi-Liang Mao-Ying, Yu-Xia Chu i 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, nr 5 (1.11.2019): 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 i Domenico Ribatti. "Vascular endothelial growth factor and vascular endothelial growth factor receptor-2 expression in mdx mouse brain". Brain Research 953, nr 1-2 (październik 2002): 12–16. http://dx.doi.org/10.1016/s0006-8993(02)03219-5.

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Ding, Yangyang, Kai Liu, Xinyu Zhao, Yingtao Lv, Rilei Yu i 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, nr 5-6 (20.01.2020): 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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Guo, Shanchun, Laronna S. Colbert, Miles Fuller, Yuanyuan Zhang i Ruben R. Gonzalez-Perez. "Vascular endothelial growth factor receptor-2 in breast cancer". Biochimica et Biophysica Acta (BBA) - Reviews on Cancer 1806, nr 1 (sierpień 2010): 108–21. http://dx.doi.org/10.1016/j.bbcan.2010.04.004.

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Sallmon, Hannes, Sandra Akanbi, Sven C. Weber, Alexander Gratopp, Cornelia Rheinländer i Petra Koehne. "Ibuprofen and indomethacin differentially regulate vascular endothelial growth factor and its receptors in ductus arteriosus endothelial cells". Cardiology in the Young 28, nr 3 (4.12.2017): 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 i 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, nr 4 (kwiecień 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 i 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, nr 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 i 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, nr 19 (10.05.1996): 11500–11505. http://dx.doi.org/10.1074/jbc.271.19.11500.

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Rozprawy doktorskie na temat "Vascular endothelial growth factor-receptor 2"

Ruch, Claudia. "Structure / function analysis of the extracellular domain of vascular endothelial growth factor receptor-2 (VEGFR-2) /". Zürich : ETH/PSI, 2007. http://e-collection.ethbib.ethz.ch/show?type=diss&nr=17030.

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Jellbauer, Stefan. "Tumorvakzinierung gegen den "Vascular Endothelial Growth Factor Receptor 2" (VEGFR2)mittels heterologem Antigentransport durch rekombinante Salmonellen". Diss., lmu, 2010. http://nbn-resolving.de/urn:nbn:de:bvb:19-120905.

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Iizuka, Takumi. "Vascular endothelial growth factor receptor 3 (VEGFR3) expression in the mouse uterus during decidualization /". Available to subscribers only, 2008. http://proquest.umi.com/pqdweb?did=1650512501&sid=1&Fmt=2&clientId=1509&RQT=309&VName=PQD.

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Higgins, Kelly Jean. "Regulation of vascular endothelial growth factor receptor-2 in pancreatic and breast cancer cells by Sp proteins". Texas A&M University, 2003. http://hdl.handle.net/1969.1/6010.

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Vascular endothelial growth factor receptor-2 (VEGFR2) is a key angiogenic factor, and angiogenesis is an important physiological process associated with neovascularization, growth, and metastasis of many different tumors. The mechanism of VEGFR2 gene expression was investigated in MiaPaCa-2, Panc-1, and AsPC-1 pancreatic cancer cells transfected with a series of VEGFR2 promoter deletion/mutated constructs, and the results indicated that the GC-rich Ã¢ÂÂ60 to Ã¢ÂÂ37 region of the promoter was essential for VEGFR2 expression in these cell lines. EMSA and ChIP assays showed that Sp proteins are expressed and bind to the proximal GC-rich region of the VEGFR2 promoter. RNA interference studies on Sp proteins demonstrated that Sp1, Sp3, and Sp4 all contributed to VEGFR2 gene/protein expression in pancreatic cancer cells. VEGFR2 gene expression was also investigated in ZR-75 and MCF-7 breast cancer cells. ZR-75 cells treated with 10 nM 17b-estradiol (E2) increased VEGFR2 mRNA levels/protein expression. The VEGFR2 promoter was induced by E2 in ZR-75 cells, and analysis of the VEGFR2 promoter identified the GC rich -60 to -37 region that was required for E2-mediated transactivation. EMSA and ChIP assays confirmed that Sp1, Sp3, and Sp4 proteins are expressed in ZR-75 cells and bind the proximal GC-rich region of the VEGFR2 promoter. RNA interference was used to determine the relative contributions of Sp proteins on hormonal regulation of VEGFR2 through ER/Sp complexes, and interestingly, in ZR-75 cells, hormone-induced activation of VEGFR2 involves ERa/Sp3 and ERa/Sp4 but not ERa/Sp1. In MCF-7 cells treated with 10 nM E2, VEGFR2 mRNA levels were decreased. Analysis of the VEGFR2 promoter revealed that the same GC-rich region important for E2-mediated upregulation in ZR-75 cells was responsible for E2-dependent downregulation of VEGFR2 gene expression in MCF-7 cells. EMSA and ChIP assays confirmed that Sp1, Sp3, and Sp4 proteins are expressed in MCF-7 cells and bind to the proximal GC-rich region of the VEGFR2 promoter. RNA interference studies showed that Sp1, Sp3, and Sp4 are involved in the E2-mediated downregulation of VEGFR2 in MCF-7 cells, and ERa/Sp protein-promoter interactions are accompanied by recruitment of the corepressor SMRT using the ChIP assay.

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Deshpande, Abhishek. "Vascular Endothelial Growth Factor Receptor-2 (VEGFR-2) and blood vessel density changes in an experimental model of Chronic Hydrocephalus". Kent State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=kent1279288736.

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Kwan, Joanne. "Induction of tumor proliferation and metastasis by expression of vascular endothelial growth factor receptor 2 in prostate carcinomas". Thesis, Boston University, 2012. https://hdl.handle.net/2144/12462.

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Thesis (M.A.)--Boston University PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
Vascular endothelial growth factor receptor 2 (VEGFR2) was first discovered on the cells of blood vessels, and has thus been referred to as an endothelial receptor. However, recent evidence suggests that some tumor cells may express VEGFR2 as well. We examine the function of the lowly metastatic human prostate cancer cell line PC3M and its highly metastatic lymph node variant PC3M-LN4. We discovered that PC3M-LN4 cells express high levels of VEGFR2. In vivo, PC3M-LN4 tumors are larger, more metastatic, and more vascularized than PC3M tumors. To further demonstrate the function of VEGFR2, PC3M cells were transfected with a VEGFR2 plasmid and G418 resistant cells were selected then grown as clones. PC3M-VEGFR2 cells were analyzed by Western blot analysis, a migration assay, and a proliferation assay. Cells expressing high levels of VEGFR2 were selected through Western blotting. A Transwell migration assay examining PC3M-VEGFR2.28 revealed greater cell migration towards VEGF-treated media as compared to VEGF-untreated media. A proliferation assay for this same clone showed greater cell proliferation with increasing concentrations of VEGF in both SF and 1% FBS media. These data suggest a direct relationship between VEGFR2 expression and tumor proliferation and metastasis. Furthermore, we noticed that an elongated cell morphology may be a characteristic of metastatic cells. Immunohistochemical analysis of prostate cancer patient biopsies reveals VEGFR2 expression on both tumor cells and endothelial cells. Interestingly, we noticed that this expression is heterogeneous between different patients and even varies within the same biopsy. Our data suggests that anti-VEGFR2 therapies may target both the tumor and blood vessels to inhibit prostate cancer disease progression in those patients that express the receptor.

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王, 英泰. "Hypoxia and vascular endothelial growth factor selectively upregulate angiopoietin-2 in bovine microvascular endothelial cells". Kyoto University, 2001. http://hdl.handle.net/2433/150200.

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Magnusson, Peetra. "Fibroblast Growth Factor Receptor-1 Function in Vasculo- and Angiogenesis". Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5824.

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Cheluvappa, Rajkumar. "Pathophysiology of Liver Sinusoidal Endothelial Cells". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/2802.

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Owing to its strategic position in the liver sinusoid, pathologic and morphologic alterations of the Liver Sinusoidal Endothelial Cell (LSEC) have far-reaching repercussions for the whole liver and systemic metabolism. LSECs are perforated with fenestrations, which are pores that facilitate the transfer of lipoproteins and macromolecules between blood and hepatocytes. Loss of LSEC porosity is termed defenestration, which can result from loss of fenestrations and/ or decreases in fenestration diameter. Gram negative bacterial endotoxin (Lipopolysaccharide, LPS) has marked effects on LSEC morphology, including induction LSEC defenestration. Sepsis is associated with hyperlipidemia, and proposed mechanisms include inhibition of tissue lipoprotein lipase and increased triglyceride production by the liver. The LSEC has an increasingly recognized role in hyperlipidemia. Conditions associated with reduced numbers of fenestrations such as ageing and bacterial infections are associated with impaired lipoprotein and chylomicron remnant uptake by the liver and consequent hyperlipidemia. Given the role of the LSEC in liver allograft rejection and hyperlipidemia, changes in the LSEC induced by LPS may have significant clinical implications. In this thesis, the following major hypotheses are explored: 1. The Pseudomonas aeruginosa toxin pyocyanin induces defenestration of the LSEC both in vitro and in vivo 2. The effects of pyocyanin on the LSEC are mediated by oxidative stress 3. Defenestration induced by old age and poloxamer 407 causes intrahepatocytic hypoxia and upregulation of hypoxia-related responses 4. Defenestration of the LSEC seen in old age can be exacerbated by diabetes mellitus and prevented or ameliorated by caloric restriction commencing early in life

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Cheluvappa, Rajkumar. "Pathophysiology of Liver Sinusoidal Endothelial Cells". University of Sydney, 2008. http://hdl.handle.net/2123/2802.

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Doctor of Philosophy(PhD)
Owing to its strategic position in the liver sinusoid, pathologic and morphologic alterations of the Liver Sinusoidal Endothelial Cell (LSEC) have far-reaching repercussions for the whole liver and systemic metabolism. LSECs are perforated with fenestrations, which are pores that facilitate the transfer of lipoproteins and macromolecules between blood and hepatocytes. Loss of LSEC porosity is termed defenestration, which can result from loss of fenestrations and/ or decreases in fenestration diameter. Gram negative bacterial endotoxin (Lipopolysaccharide, LPS) has marked effects on LSEC morphology, including induction LSEC defenestration. Sepsis is associated with hyperlipidemia, and proposed mechanisms include inhibition of tissue lipoprotein lipase and increased triglyceride production by the liver. The LSEC has an increasingly recognized role in hyperlipidemia. Conditions associated with reduced numbers of fenestrations such as ageing and bacterial infections are associated with impaired lipoprotein and chylomicron remnant uptake by the liver and consequent hyperlipidemia. Given the role of the LSEC in liver allograft rejection and hyperlipidemia, changes in the LSEC induced by LPS may have significant clinical implications. In this thesis, the following major hypotheses are explored: 1. The Pseudomonas aeruginosa toxin pyocyanin induces defenestration of the LSEC both in vitro and in vivo 2. The effects of pyocyanin on the LSEC are mediated by oxidative stress 3. Defenestration induced by old age and poloxamer 407 causes intrahepatocytic hypoxia and upregulation of hypoxia-related responses 4. Defenestration of the LSEC seen in old age can be exacerbated by diabetes mellitus and prevented or ameliorated by caloric restriction commencing early in life

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Książki na temat "Vascular endothelial growth factor-receptor 2"

Duman, Ronald S. Neurotrophic Mechanisms of Depression. Redaktorzy Dennis S. Charney, Eric J. Nestler, Pamela Sklar i Joseph D. Buxbaum. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190681425.003.0027.

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Early theories of depression and treatment response were centered on the monoamine neurotransmitters, but more recent work has focused on functional and structural synaptic plasticity and the role of neurotrophic factors, particularly brain derived neurotrophic factor (BDNF). Neurotrophic factors regulate all aspects of neuronal function, including adaptive plasticity, synapse formation, and neuronal survival. Chronic stress and depression cause reductions in levels of BDNF and other key factors, including vascular endothelial growth factor (VEGF) and fibroblast growth factor 2 (FGF2), in cortical regions that contribute to atrophy and loss of neurons observed in depressed patients and rodent stress models. In contrast, these neurotrophic factors are upregulated by chronic administration of typical antidepressants and are required for antidepressant responses. Moreover, fast acting, highly efficacious antidepressant agents such as ketamine rapidly increase BDNF release and synapse formation, paving the way for a new generation of medications for the treatment of depression.

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Badimon, Lina, i Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0040.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the extracellular matrix and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated monocytes differentiate into macrophages which acquire a specialized phenotypic polarization (protective or harmful), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoprotein via low-density lipoprotein receptor-related protein-1 receptors. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Both lipid-laden vascular smooth muscle cells and macrophages release the procoagulant tissue factor, contributing to thrombus propagation. Platelets also participate in progenitor cell recruitment and drive the inflammatory response mediating the atherosclerosis progression. Recent data attribute to microparticles a potential modulatory effect in the overall atherothrombotic process. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be modulated.

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Alharbi, Yousef, Manish S. Patankar i Rebecca J. Whelan. Antibody-Based Therapy for Ovarian Cancer. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190248208.003.0006.

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With their role in connecting disease-associated antigens to the cellular immune response, antibodies hold considerable promise as therapeutic agents. This chapter discusses three classes of therapeutic antibodies that have been developed for use in ovarian cancer therapy. The first includes antibodies selected against tumor-associated antigens such as MUC16/CA125, mesothelin, epithelial cell adhesion molecule, and folate receptor α‎. Antibodies in the second class target proteins such as CTLA-4 and PD1 that act as immune response checkpoint receptors. The third class of antibodies target secreted factors that promote tumor growth: targets in this class include vascular endothelial growth factor, cytokines, and chemokines. The development of each of these is described. The chapter also discusses the complications presented by soluble antigens, which serve to limit the applicability of antigens (such as MUC16/CA125) that are both cell-surface associated and circulating and the prospects for the combination of antibody-based immunotherapy and chemotherapy.

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Badimon, Lina, i Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_001.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

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Badimon, Lina, i Gemma Vilahur. Atherosclerosis and thrombosis. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0040_update_002.

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Atherosclerosis is the main underlying cause of heart disease. The continuous exposure to cardiovascular risk factors induces endothelial activation/dysfunction which enhances the permeability of the endothelial layer and the expression of cytokines/chemokines and adhesion molecules. This results in the accumulation of lipids (low-density lipoprotein particles) in the intimal layer and the triggering of an inflammatory response. Accumulated low-density lipoprotein particles attached to the extracellular matrix suffer modifications and become pro-atherogenic, enhancing leucocyte recruitment and further transmigration across the endothelium into the intima. Infiltrated pro-atherogenic monocytes (mainly Mon2) differentiate into macrophages which acquire a specialized phenotypic polarization (protective/M1 or harmful/M2), depending on the stage of the atherosclerosis progression. Once differentiated, macrophages upregulate pattern recognition receptors capable of engulfing modified low-density lipoprotein, leading to foam cell formation. Foam cells release growth factors and cytokines that promote vascular smooth muscle cell migration into the intima, which then internalize low-density lipoproteins via low-density lipoprotein receptor-related protein-1 receptors becoming foam cells. As the plaque evolves, the number of vascular smooth muscle cells decline, whereas the presence of fragile/haemorrhagic neovessels and calcium deposits increases, promoting plaque destabilization. Disruption of this atherosclerotic lesion exposes thrombogenic surfaces rich in tissue factor that initiate platelet adhesion, activation, and aggregation, as well as thrombin generation. Platelets also participate in leucocyte and progenitor cell recruitment are likely to mediate atherosclerosis progression. Recent data attribute to microparticles a modulatory effect in the overall atherothrombotic process and evidence their potential use as systemic biomarkers of thrombus growth. This chapter reviews our current understanding of the pathophysiological mechanisms involved in atherogenesis, highlights platelet contribution to thrombosis and atherosclerosis progression, and provides new insights into how atherothrombosis may be prevented and modulated.

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Części książek na temat "Vascular endothelial growth factor-receptor 2"

Marmé, Dieter. "Vascular Endothelial Growth Factor". W Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_6155-2.

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Shibuya, M., N. Ito i L. Claesson-Welsh. "Structure and Function of Vascular Endothelial Growth Factor Receptor-1 and -2". W Current Topics in Microbiology and Immunology, 59–83. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59953-8_4.

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Tonra, James R., Marie Prewett, Erik Corcoran, Daniel J. Hicklin i Zhenping Zhu. "In Vivo Method for Establishing Synergy Between Antibodies to Epidermal Growth Factor Receptor and Vascular Endothelial Growth Factor Receptor-2". W Therapeutic Antibodies, 545–57. Totowa, NJ: Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-554-1_30.

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Paz, Keren, i Zhenping Zhu. "Development of Angiogenesis Inhibitors to Vascular Endothelial Growth Factor Receptor 2 for Cancer Therapy". W Topics in Medicinal Chemistry, 333–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2007. http://dx.doi.org/10.1007/7355_2006_009.

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Ferrara, Napoleone, John E. Park, Claire E. Walder, Stuart Bunting i G. Roger Thomas. "The Regulation of Normal and Pathological Angiogenesis by Vascular Endothelial Growth Factor". W Cardiovascular Disease 2, 133–44. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1959-1_18.

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Zheng, Yongqiang, Jianfen Wei, Xiaojun Li, Ling Xue i Guoyu Qiao. "Detection of Serum Vascular Endothelial Growth Factor (VEGF) and Endothelin, in Type 2 Diabetic Nephropathy Patients and Its Clinical Significance". W Lecture Notes in Electrical Engineering, 1387–92. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-2169-2_165.

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Ferrario, Angela, i Charles J. Gomer. "Targeting the Tumor Microenvironment Using Photodynamic Therapy Combined with Inhibitors of Cyclooxygenase-2 or Vascular Endothelial Growth Factor". W Methods in Molecular Biology, 121–32. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-697-9_9.

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Lugano, Roberta, Hua Huang i Anna Dimberg. "Vascular Endothelial Growth Factor Receptor (VEGFR)". W Encyclopedia of Signaling Molecules, 5884–92. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101914.

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Taipale, J., T. Makinen, E. Arighi, E. Kukk, M. Karkkainen i K. Alitalo. "Vascular Endothelial Growth Factor Receptor-3". W Current Topics in Microbiology and Immunology, 85–96. Berlin, Heidelberg: Springer Berlin Heidelberg, 1999. http://dx.doi.org/10.1007/978-3-642-59953-8_5.

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Lugano, Roberta, Hua Huang i Anna Dimberg. "Vascular Endothelial Growth Factor Receptor (VEGFR)". W Encyclopedia of Signaling Molecules, 1–9. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101914-1.

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Streszczenia konferencji na temat "Vascular endothelial growth factor-receptor 2"

Mitsunaga, Makoto, Takashi Nishimura i Kimihiro Ito. "Abstract 5767: Vascular endothelial growth factor receptor 2 targeted photoimmunotherapy". W Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5767.

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Chandler, Kevin B., Deborah R. Leon, Rosana D. Meyer, Nader Rahimi i Catherine E. Costello. "Abstract 1808: Vascular endothelial growth factor receptor-2 (VEGFR-2)N-glycosylation modulates angiogenic signaling". W Proceedings: AACR Annual Meeting 2017; April 1-5, 2017; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-1808.

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Kubo, Toshio, Kadoaki Ohashi, Masahiro Osawa, Hiromasa Takeda, Eiki Ichihara, Takashi Ninomiya, Nagio Takigawa i in. "Abstract 3681: Vascular endothelial growth factor receptor tyrosine kinase inhibitor inhibited mutated epidermal growth factor receptor-driven tumors ex vivo and in vivo". W 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.am2011-3681.

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Zebda, Noureddine, Tiffany Ho, Nurgul Moldobaeva, Anna Birukova, Judith A. Berliner i Konstantin G. Birukov. "Involvement Of Vascular Endothelial Growth Factor Receptor 2 (VEGFR2) In Oxidized Phospholipid-Mediated Control Of Endothelial Barrier Function". W 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.a1974.

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Cerri, Elisa, Sonal Kashyap, Pei Xian Chen, Soma Das, Nicole Cipriani, Rajani Kanteti, Aliya Husain, Ravi Salgia i Federico Innocenti. "Abstract 2176: Vascular endothelial growth factor receptor-2 (VEGFR-2) gene variations in bronchioloalveolar cell carcinoma (BAC)". W 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.am10-2176.

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Alekperov, R., E. Alexandrova, A. Novikov i L. Ananyeva. "AB0798 Clinical associations of vascular endothelial growth factor and its receptor 2 type in systemic sclerosis". W Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.4064.

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Lee, You Mie, Jiyoon Seok, Soo-Hyun Yoon, Sun-Hee Lee i Jong Hwa Jung. "Abstract 188: The oncometabolite d-2-hydroxyglutarate induces angiogenic activity through the vascular endothelial growth factor receptor 2 signaling pathway". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-188.

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Kim, Hee Sung, Hye Seung Lee i Woo Ho Kim. "Abstract 5576: pmTOR and vascular endothelial growth factor receptor (VEGFR)-2 expressions in gastroenteropancreatic neuroendocrine tumors (GEP-NETs)". W Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5576.

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Morss, Alisa, Michael Jonas i Elazer R. Edelman. "Elevated Basement Membrane Fibroblast Growth Factor-2 Protects Endothelial Cells in High Glucose". W ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176187.

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Streszczenie:

Vascular disease is the primary cause of morbidity and mortality in diabetics. Diabetic vascular disease is disseminated and includes renal capillary hypertrophy, reduced wound repair, impaired angiogenesis, and rapid and excessive hyperplasia after endovascular intervention [1, 2]. No single biochemical aberration unifies the diffuse nature of diabetic vascular disease. Hyperglycemia has been implicated, and yet glucose effects persist long after restoration of euglycemia. It is possible that acute fluctuations in glucose concentration have prolonged cell and tissue effects.

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Raporty organizacyjne na temat "Vascular endothelial growth factor-receptor 2"

Li, Ting, Shudan Ge, Wei Zheng, Chao Luan, Xingtong Liu, Zongxiu Luo, Qi Zhao i Lulu Xie. Effectiveness and safety of panretinal photocoagulation combined with intravitreous ranibizumab for patients with type 2 proliferative diabetic retinopathy：A protocol for systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, kwiecień 2022. http://dx.doi.org/10.37766/inplasy2022.4.0048.

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Review question / Objective: Our study aims to synthesise results from randomised controlled trials to assess the effectiveness and safety of PRP combined with intravitreous ranibizumab for T2PDR. Condition being studied: Diabetic retinopathy (DR) is the most common complication of diabetes mellitus, which will seriously affect the quality of life of patients and bring great burden to patients’ families and society. DR is one of the most important diseases of blindness in people aged 20 to 60 years worldwide. Nearly 15% of diabetic patients with a disease duration of more than 5 years were combined with DR.The prevalence of vision threatening diabetic retinopathy in the United States is 4.4 percent. Worldwide, the prevalence is estimated at 10.2%.At present, the treatment methods for type 2 proliferative diabetic retinopathy (T2PDR), at home and abroad mainly include retinal laser photocoagulation and intravitreal injection of vascular endothelial growth factor (VEGF) inhibitors.

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Tan, Linlin, Zhijie Wang, Yuchun Ni, Fupeng Zhang, Zhaowei Huang, Zhipeng Zhang, Jiaqi Yan i Mei Wu. The efficacy and safety of vascular endothelial growth factor receptor (VEGFR ) inhibitors for recurrent ovarian cancer: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, luty 2021. http://dx.doi.org/10.37766/inplasy2021.2.0019.

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