Suppression of Retinal Neovascularization With an Antagonist to Vascular Endothelial Cadherin

Navaratna, Deepti

doi:10.1001/archopht.126.8.1082

Cited by 10 publications

(11 citation statements)

References 32 publications

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“…It has been shown previously that blocking a different adhesive protein, R-cadherin, inhibits retinal angiogenesis 54 . Inhibition of the endothelial cell adhesion protein VE-cadherin also suppresses neovessel sprouting and angiogenesis 55-58 . Similarly, Cln5 may be necessary for cell-cell adhesion, endothelial cell migration and tube formation and thus would play an essential role for the proper growth of vascular sprouts and vessel growth.…”

Section: Discussionmentioning

confidence: 99%

Wnt Signaling Mediates Pathological Vascular Growth in Proliferative Retinopathy

et al. 2011

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Background Ischemic proliferative retinopathy, characterized by pathologic retinal neovascularization, is a major cause of blindness in working age adults and children. Defining the molecular pathways distinguishing pathological neovascularization from normal vessels is critical to controlling these blinding diseases with targeted therapy. Because mutations in Wnt signaling cause defective retinal vasculature in humans with some characteristics of the pathologic vessels in retinopathy, we investigated the potential role of Wnt signaling in pathologic retinal vascular growth in proliferative retinopathy. Methods and Results In this study we show that Wnt receptors (Frizzled4 and Lrp5) and activity are significantly increased in pathologic neovascularization in a mouse model of oxygen-induced proliferative retinopathy. Loss of Wnt co-receptor Lrp5 and downstream signaling molecule disheveled2 significantly decreases the formation of pathologic retinal neovascularization in retinopathy. Loss of Lrp5 also affects retinal angiogenesis during development and formation of the blood retinal barrier, which is linked to significant down-regulation of tight junction protein claudin5 (Cln5) in Lrp5−/− vessels. Blocking Cln5 significantly suppresses Wnt-pathway driven endothelial cell sprouting in vitro and developmental and pathologic vascular growth in retinopathy in vivo. Conclusions These results demonstrate an important role of Wnt signaling in pathologic vascular development in retinopathy and show a novel function of Cln5 in promoting angiogenesis.

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Section: Discussionmentioning

confidence: 99%

Wnt Signaling Mediates Pathological Vascular Growth in Proliferative Retinopathy

et al. 2011

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“…This therapy is antiangiogenic during neovascularization because de novo adherens junction formation is inhibited. The potential value of anti-VE-cadherin therapy was further shown by using a cyclic peptide directed against VEcadherin to inhibit oxygen-induced retinal neovascularization (Navaratna et al 2008). Regarding angiogenesis, it is worth mentioning that endothelial cells also express N-cadherin, R-cadherin (CDH4), and T-cadherin (cadherin-13; see the following discussion).…”

Section: Ve-cadherin (Cadherin-5) and Other Type-ii Cadherinsmentioning

confidence: 99%

Involvement of Members of the Cadherin Superfamily in Cancer

Berx¹,

Roy²

2009

Cold Spring Harbor Perspectives in Biology

568

489

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We review the role of cadherins and cadherin-related proteins in human cancer. Cellular and animal models for human cancer are also dealt with whenever appropriate. E-cadherin is the prototype of the large cadherin superfamily and is renowned for its potent malignancy suppressing activity. Different mechanisms for inactivating E-cadherin/CDH1 have been identified in human cancers: inherited and somatic mutations, aberrant protein processing, increased promoter methylation, and induction of transcriptional repressors such as Snail and ZEB family members. The latter induce epithelial mesenchymal transition, which is also associated with induction of "mesenchymal" cadherins, a hallmark of tumor progression. VE-cadherin/CDH5 plays a role in tumor-associated angiogenesis. The atypical T-cadherin/ CDH13 is often silenced in cancer cells but up-regulated in tumor vasculature. The review also covers the status of protocadherins and several other cadherin-related molecules in human cancer. Perspectives for emerging cadherin-related anticancer therapies are given.

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“…Most of the works isolated BRECs from bovine eyes, using previously described protocols. Only a few authors affirm to have purchased the cells from banks [ 21 , 29 ]. For the experiments, cells were used from one passage in minimum [ 32 , 33 ] to 15 in maximum [ 15 ], which is important since this is a primary culture and not an immortalized cell line.…”

Section: Cell Culturementioning

confidence: 99%

A Critical Analysis of the AvailableIn VitroandEx VivoMethods to Study Retinal Angiogenesis

Moleiro

Conceição

Leite‐Moreira

et al. 2017

Journal of Ophthalmology

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Angiogenesis is a biological process with a central role in retinal diseases. The choice of the ideal method to study angiogenesis, particularly in the retina, remains a problem. Angiogenesis can be assessed through in vitro and in vivo studies. In spite of inherent limitations, in vitro studies are faster, easier to perform and quantify, and typically less expensive and allow the study of isolated angiogenesis steps. We performed a systematic review of PubMed searching for original articles that applied in vitro or ex vivo angiogenic retinal assays until May 2017, presenting the available assays and discussing their applicability, advantages, and disadvantages. Most of the studies evaluated migration, proliferation, and tube formation of endothelial cells in response to inhibitory or stimulatory compounds. Other aspects of angiogenesis were studied by assessing cell permeability, adhesion, or apoptosis, as well as by implementing organotypic models of the retina. Emphasis is placed on how the methods are applied and how they can contribute to retinal angiogenesis comprehension. We also discuss how to choose the best cell culture to implement these methods. When applied together, in vitro and ex vivo studies constitute a powerful tool to improve retinal angiogenesis knowledge. This review provides support for researchers to better select the most suitable protocols in this field.

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Suppression of Retinal Neovascularization With an Antagonist to Vascular Endothelial Cadherin

Cited by 10 publications

References 32 publications

Wnt Signaling Mediates Pathological Vascular Growth in Proliferative Retinopathy

Wnt Signaling Mediates Pathological Vascular Growth in Proliferative Retinopathy

Involvement of Members of the Cadherin Superfamily in Cancer

A Critical Analysis of the AvailableIn VitroandEx VivoMethods to Study Retinal Angiogenesis

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