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Title:
VEGF-C differentially regulates VEGF-A expression in ocular and cancer cells; promotes angiogenesis via RhoA mediated pathway | Angiogenesis
Description:
Vascular angiogenesis is regulated by a number of cytokines of which vascular endothelial growth factor (VEGF)-A/and its receptor vascular endothelial growth factor receptor 2 (VEGFR2) play an indisputable role. Similarly lymphangiogenesis is regulated by VEGF-C and its receptor VEGFR3. Currently for treating vasculogenesis diseases such as proliferative retinopathies and cancer, a number of anti-VEGF-A therapies are approved for clinical use. Although clinical efficacies achieved are remarkable, they are found to be transitory in nature, followed by restoration of anti-VEGF therapy resistant angiogenesis. Recently the regulatory role of VEGF-C in initiating and potentiating neo-angiogenesis has been uncovered. Although the interactive nature of VEGF-A and C is known, the dynamics of their expression under knockdown conditions is yet to be established. Here in this study we have utilized siRNA to knockdown both VEGF-A and C either independently or in combination. Analysis of VEGF-A and C expression (only in cancer cell lines MCF7, A549 and H460 but not in the ocular cell line RPE19) has shown enhanced expression levels of VEGF-C with increase in knockdown of VEGF-A. However, VEGF-C knockdown has resulted in decreased expression levels of VEGF-A both in RPE19 and MCF7 cells in a dose dependent manner. In addition, VEGF-C knockdown also resulted in decreased expression of RhoA. Further, knockdown studies of RhoA even with supplementation of VEGF-C or A has resulted in decreased endothelial cell proliferation and stress fiber formation, indicating that VEGF-C does promote angiogenesis via RhoA mediated pathway.
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article, google, scholar, angiogenesis, pubmed, cas, cancer, endothelial, vegfc, vascular, growth, factor, cell, vegfa, expression, kumar, nature, knockdown, tumor, promotes, rhoa, receptor, therapy, sci, privacy, cookies, content, regulates, cells, mediated, lymphangiogenesis, access, res, life, information, publish, research, search, chile, ray, addepalli, role, conditions, human, sciences, data, log, journal, ocular, pathway,
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venkata ramana & vikram rajagopal month download article/chapter anti-angiogenic factor pedf rhoa/rho kinase signaling article angiogenesis aims full article pdf reliance life sciences human tumor angiogenesis intralymphatic tumor growth privacy choices/manage cookies gene ther 17 rhoa mediated pathway anti angiogenic therapy retinalvascular endothelial cells vascular network formation rho activity critically elevated cell invasion potentiating neo-angiogenesis /vegf receptor system rho signaling prostate tumor regression young diabetic patients streptozotocin diabetic rat vikram rajagopal related subjects promotes tumor lymphangiogenesis european economic area stress fiber formation quantitative vitreaous fluorophotometry measuring early breakdown blood-tretinal barrier hull-campbell ne cyclin-dependent kinases syndecan-4 signals cooperatively actin stress fibers authors gratefully acknowledge thane-belapur road rnai mediated knockdown primary breast cancer dose dependent manner freeze fracture studies pre-malignant conditions differentially regulates vegf electronic supplementary material decreased expression levels conditions privacy policy accepting optional cookies treating vasculogenesis diseases clinical efficacies achieved author information authors
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- Folkman J (2007) Angiogenesis: an organizing principle for drug discovery?
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headline:VEGF-C differentially regulates VEGF-A expression in ocular and cancer cells; promotes angiogenesis via RhoA mediated pathway
description:Vascular angiogenesis is regulated by a number of cytokines of which vascular endothelial growth factor (VEGF)-A/and its receptor vascular endothelial growth factor receptor 2 (VEGFR2) play an indisputable role. Similarly lymphangiogenesis is regulated by VEGF-C and its receptor VEGFR3. Currently for treating vasculogenesis diseases such as proliferative retinopathies and cancer, a number of anti-VEGF-A therapies are approved for clinical use. Although clinical efficacies achieved are remarkable, they are found to be transitory in nature, followed by restoration of anti-VEGF therapy resistant angiogenesis. Recently the regulatory role of VEGF-C in initiating and potentiating neo-angiogenesis has been uncovered. Although the interactive nature of VEGF-A and C is known, the dynamics of their expression under knockdown conditions is yet to be established. Here in this study we have utilized siRNA to knockdown both VEGF-A and C either independently or in combination. Analysis of VEGF-A and C expression (only in cancer cell lines MCF7, A549 and H460 but not in the ocular cell line RPE19) has shown enhanced expression levels of VEGF-C with increase in knockdown of VEGF-A. However, VEGF-C knockdown has resulted in decreased expression levels of VEGF-A both in RPE19 and MCF7 cells in a dose dependent manner. In addition, VEGF-C knockdown also resulted in decreased expression of RhoA. Further, knockdown studies of RhoA even with supplementation of VEGF-C or A has resulted in decreased endothelial cell proliferation and stress fiber formation, indicating that VEGF-C does promote angiogenesis via RhoA mediated pathway.
datePublished:2011-06-23T00:00:00Z
dateModified:2011-06-23T00:00:00Z
pageStart:371
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sameAs:https://doi.org/10.1007/s10456-011-9221-5
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VEGF-C
VEGF-A
siRNA
RhoA
Cancer
Cancer Research
Biomedicine
general
Cell Biology
Cardiology
Ophthalmology
Oncology
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headline:VEGF-C differentially regulates VEGF-A expression in ocular and cancer cells; promotes angiogenesis via RhoA mediated pathway
description:Vascular angiogenesis is regulated by a number of cytokines of which vascular endothelial growth factor (VEGF)-A/and its receptor vascular endothelial growth factor receptor 2 (VEGFR2) play an indisputable role. Similarly lymphangiogenesis is regulated by VEGF-C and its receptor VEGFR3. Currently for treating vasculogenesis diseases such as proliferative retinopathies and cancer, a number of anti-VEGF-A therapies are approved for clinical use. Although clinical efficacies achieved are remarkable, they are found to be transitory in nature, followed by restoration of anti-VEGF therapy resistant angiogenesis. Recently the regulatory role of VEGF-C in initiating and potentiating neo-angiogenesis has been uncovered. Although the interactive nature of VEGF-A and C is known, the dynamics of their expression under knockdown conditions is yet to be established. Here in this study we have utilized siRNA to knockdown both VEGF-A and C either independently or in combination. Analysis of VEGF-A and C expression (only in cancer cell lines MCF7, A549 and H460 but not in the ocular cell line RPE19) has shown enhanced expression levels of VEGF-C with increase in knockdown of VEGF-A. However, VEGF-C knockdown has resulted in decreased expression levels of VEGF-A both in RPE19 and MCF7 cells in a dose dependent manner. In addition, VEGF-C knockdown also resulted in decreased expression of RhoA. Further, knockdown studies of RhoA even with supplementation of VEGF-C or A has resulted in decreased endothelial cell proliferation and stress fiber formation, indicating that VEGF-C does promote angiogenesis via RhoA mediated pathway.
datePublished:2011-06-23T00:00:00Z
dateModified:2011-06-23T00:00:00Z
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VEGF-C
VEGF-A
siRNA
RhoA
Cancer
Cancer Research
Biomedicine
general
Cell Biology
Cardiology
Ophthalmology
Oncology
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