Increased Migration by Stimulation of Thymidine Phosphorylase in Endothelial Cells of Different Origin

Bijnsdorp, Irene V.; Vrijland, Kim; Vroling, Laura; Fukushima, Masakazu; Peters, Godefridus J.

doi:10.1080/15257771003730201

Cited by 6 publications

(7 citation statements)

References 15 publications

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“…TP expression in endothelial cells may also be important for their angiogenic properties. However, TP expression is very low in endothelial cells [43,44]. In A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 14 autocrine stimulation by endothelial cells themselves.…”

Section: Discussionmentioning

confidence: 98%

Accumulation of thymidine-derived sugars in thymidine phosphorylase overexpressing cells

Bijnsdorp

Azijli

Jansen

et al. 2010

Biochemical Pharmacology

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Section: Discussionmentioning

confidence: 98%

Accumulation of thymidine-derived sugars in thymidine phosphorylase overexpressing cells

Bijnsdorp

Azijli

Jansen

et al. 2010

Biochemical Pharmacology

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“…HUVEC migration was assessed using the wound-healing assay as previously described [ 20 , 21 ]. HUVECs were seeded (1×10 5 cells/well) in duplicate to 1% gelatin-coated 24-well plates (Corning, Schiphol, Netherlands).…”

Section: Methodsmentioning

confidence: 99%

Therapeutic Effects of Topical Netrin-4 Inhibits Corneal Neovascularization in Alkali-Burn Rats

et al. 2015

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Netrins are secreted molecules involved in axon guidance and angiogenesis. However, the role of netrins in the vasculature remains unclear. Netrin-4 and netrin-1 have been found to be either pro- or antiangiogenic factors. Previously, we found that netrin-1 acts as an anti-angiogenic factor in rats by inhibiting alkali burn-induced corneal neovascularization. Here, we further investigate the effects of netrin-4, another member of the same netrin family, on neovascularization in vitro and in vivo. We found that netrin-4 functions similarly as netrin-1 in angiogenesis. In vitro angiogenesis assay shows that netrin-4 affected human umbilical vein endothelial cell (HUVEC) tube formation, viability and proliferation, apoptosis, migration, and invasion in a dose-dependent manner. Netrin-4 was topically applied in vivo to alkali-burned rat corneas on day 0 (immediately after injury) and/or day 10 post-injury. Netrin-4 subsequently suppressed and reversed corneal neovascularization. Netrin-4 inhibited corneal epithelial and stromal cell apoptosis, inhibited vascular endothelial growth factor (VEGF), but promoted pigment epithelium-derived factor (PEDF) expression, decreased NK-KB p65 expression, and inhibits neutrophil and macrophage infiltration. These results indicate that netrin-4 shed new light on its potential roles in treatmenting for angiogenic diseases that affect the ocular surface, as well as other tissues.

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“…Human umbilical vein endothelial cell migration was determined using the wound healing assay as described previously (Bijman et al , 2006; Bijnsdorp et al , 2010b). Human umbilical vein endothelial cells were seeded (100 000 cells per well) in duplicates in 1% gelatin coated wells of a 24 wells plate (Corning, Schiphol, The Netherland).…”

Section: Methodsmentioning

confidence: 99%

Thymidine phosphorylase in cancer cells stimulates human endothelial cell migration and invasion by the secretion of angiogenic factors

et al. 2011

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Background:Thymidine phosphorylase (TP) is often overexpressed in tumours and has a role in tumour aggressiveness and angiogenesis. Here, we determined whether TP increased tumour invasion and whether TP-expressing cancer cells stimulated angiogenesis.Methods:Angiogenesis was studied by exposing endothelial cells (HUVECs) to conditioned medium (CM) derived from cancer cells with high (Colo320TP1=CT-CM, RT112/TP=RT-CM) and no TP expression after which migration (wound-healing-assay) and invasion (transwell-assay) were determined. The involvement of several angiogenic factors were examined by RT–PCR, ELISA and blocking antibodies.Results:Tumour invasion was not dependent on intrinsic TP expression. The CT-CM and RT-CM stimulated HUVEC-migration and invasion by about 15 and 40%, respectively. Inhibition by 10 μ TPI and 100 μ L-dR, blocked migration and reduced the invasion by 50–70%. Thymidine phosphorylase activity in HUVECs was increased by CT-CM. Reverse transcription-polymerase chain reaction revealed a higher mRNA expression of bFGF (Colo320TP1), IL-8 (RT112/TP) and TNF-α, but not VEGF. Blocking antibodies targeting these factors decreased the migration and invasion that was induced by the CT-CM and RT-CM, except for IL-8 in CT-CM and bFGF in RT-CM.Conclusion:In our cell line panels, TP did not increase the tumour invasion, but stimulated the migration and invasion of HUVECs by two different mechanisms. Hence, TP targeting seems to provide a potential additional strategy in the field of anti-angiogenic therapy.

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Increased Migration by Stimulation of Thymidine Phosphorylase in Endothelial Cells of Different Origin

Cited by 6 publications

References 15 publications

Accumulation of thymidine-derived sugars in thymidine phosphorylase overexpressing cells

Accumulation of thymidine-derived sugars in thymidine phosphorylase overexpressing cells

Therapeutic Effects of Topical Netrin-4 Inhibits Corneal Neovascularization in Alkali-Burn Rats

Thymidine phosphorylase in cancer cells stimulates human endothelial cell migration and invasion by the secretion of angiogenic factors

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