Involvement of lysosomal degradation in VEGF‐C‐induced down‐regulation of VEGFR‐3

Han, Kunsoo; Chang, Jin Hong; Dugas-Ford, Jennifer; Alexander, J. Steven; Azar, Dimitri T.

doi:10.1016/j.febslet.2014.09.034

Cited by 15 publications

(14 citation statements)

References 44 publications

(50 reference statements)

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“…Endostatin inhibits angiogenesis by directly binding to both VEGFR-1 and VEGFR-2 and blocking VEGF interaction with Flt-1 and Flk-1 to prevent VEGF-induced tyrosine phosphorylation of VEGFR-1 and VEGFR-2 and all downstream signaling events [102]. VEGFR-3 (also known as flt-4), another receptor tyrosine kinase, is expressed primarily on lymphatic endothelial cell surfaces [103]. Endostatin competitively inhibits VEGF binding to VEGFR-3 in vitro [104].…”

Section: Endostatin Receptorsmentioning

confidence: 99%

Endostatin's emerging roles in angiogenesis, lymphangiogenesis, disease, and clinical applications

Walia

Yang

Huang

et al. 2015

Biochimica et Biophysica Acta (BBA) - General Subjects

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153

126

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Background Angiogenesis is the process of neovascularization from pre-existing vasculature and is involved in various physiological and pathological processes. Inhibitors of angiogenesis, administered either as individual drugs or in combination with other chemotherapy, have been shown to benefit patients with various cancers. Endostatin, a 20-kDa C-terminal fragment of type XVIII collagen, is one of the most potent inhibitors of angiogenesis. Scope of review We discuss the biology behind endostatin in the context of its endogenous production, the various receptors to which it binds, and the mechanisms by which it acts. We focus on its inhibitory role in angiogenesis, lymphangiogenesis, and cancer metastasis. We also present emerging clinical applications for endostatin and its potential as a therapeutic agent in the form a short peptide. Major conclusions The delicate balance between pro- and anti-angiogenic factors can be modulated to result in physiological wound healing or pathological tumor metastasis. Research in the last decade has emphasized an emerging clinical potential for endostatin as a biomarker and as a therapeutic short peptide. Moreover, elevated or depressed endostatin levels in diseased states may help explain the pathophysiological mechanisms of the particular disease. General significance Endostatin was once sought after as the ‘be all and end all’ for cancer treatment; however, research throughout the last decade has made it apparent that endostatin’s effects are complex and involve multiple mechanisms. A better understanding of newly discovered mechanisms and clinical applications still has the potential to lead to future advances in the use of endostatin in the clinic.

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Section: Endostatin Receptorsmentioning

confidence: 99%

Endostatin's emerging roles in angiogenesis, lymphangiogenesis, disease, and clinical applications

Walia

Yang

Huang

et al. 2015

Biochimica et Biophysica Acta (BBA) - General Subjects

Self Cite

153

126

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“…The corneal epithelium produces both pro- and anti-angiogenic factors. The secreted forms of VEGFR-1, -2 and -3 are also produced in the corneal epithelium [30–33]. The VEGFR family is involved in both HA and LA, depending on the receptor subtype.…”

Section: Discussionmentioning

confidence: 99%

Limited versus total epithelial debridement ocular surface injury: Live fluorescence imaging of hemangiogenesis and lymphangiogenesis in Prox1-GFP/Flk1::Myr-mCherry mice

Chang

Putra

Huang

et al. 2016

Biochimica et Biophysica Acta (BBA) - General Subjects

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Background Immunohistochemical staining experiments have shown that both hemangiogenesis and lymphangiogenesis occur following severe corneal and conjunctival injury and that the neovascularization of the cornea often has severe visual consequences. To better understand how hemangiogenesis and lymphangiogenesis are induced by different degrees of ocular injury, we investigated patterns of injury-induced corneal neovascularization in live Prox1-GFP/Flk1::myr-mCherry mice, in which blood and lymphatic vessels can be imaged simultaneously in vivo. Methods The eyes of Prox1-GFP/Flk1::myr-mCherry mice were injured according to four models based on epithelial debridement of the: A) central cornea (a 1.5-mm-diameter circle of tissue over the corneal apex), B) total cornea, C) bulbar conjunctiva, and D) cornea+bulbar conjunctiva. Corneal blood and lymphatic vessels were imaged on days 0, 3, 7, and 10 post-injury, and the percentages of the cornea containing blood and lymphatic vessels were calculated. Results Neither central corneal nor bulbar conjunctival debridement resulted in significant vessel growth in the mouse cornea, whereas total corneal and corneal+bulbar conjunctival debridement did. On day 10 in the central cornea, total cornea, bulbar conjunctiva, and corneal+bulbar conjunctival epithelial debridement models, the percentage of the corneal surface that was occupied by blood vessels (hemangiogenesis) was 1.9±0.8%, 7.14±2.4%, 2.29±1%, and 15.05±2.14%, respectively, and the percentage of the corneal surface that was occupied by lymphatic vessels (lymphangiogenesis) was 2.45±1.51%, 4.85±0.95%, 2.95±1.27%, and 4.15±3.85%, respectively. Conclusions Substantial corneal debridement was required to induce corneal neovascularization in the mouse cornea, and the corneal epithelium may therefore be partially responsible for maintaining corneal avascularity. General significance Our study demonstrates that GFP/Flk1::myr-mCherry mice are a useful model for studying coordinated hemangiogenic and lymphangiogenic responses.

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“…Endostatin binds both endogenous angiogenesis inhibitors thrombospondin-1 and SPARC (544, 545) and upregulates thrombospondin-1 expression (546). Endostatin also binds VEGFR2 on EC and VEGFR3 on lymphatic vessels preventing activation and downstream signaling (533,547,548). By occupying integrin-ECM binding sites, initiation of the tyrosine phosphorylation cascade, src activation, and EC migration are interrupted (549,550).…”

Section: Angiogenesis In Pancreatic Cancermentioning

confidence: 99%

Ping-Pong—Tumor and Host in Pancreatic Cancer Progression

Wang

Zöller

2019

Front. Oncol.

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Involvement of lysosomal degradation in VEGF‐C‐induced down‐regulation of VEGFR‐3

Cited by 15 publications

References 44 publications

Endostatin's emerging roles in angiogenesis, lymphangiogenesis, disease, and clinical applications

Endostatin's emerging roles in angiogenesis, lymphangiogenesis, disease, and clinical applications

Limited versus total epithelial debridement ocular surface injury: Live fluorescence imaging of hemangiogenesis and lymphangiogenesis in Prox1-GFP/Flk1::Myr-mCherry mice

Ping-Pong—Tumor and Host in Pancreatic Cancer Progression

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