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- W3103264823 abstract "Background Vascular changes are consistent early findings in SSc and often proceed the development of fibrosis. Despite a severe reduction in the capillary density, signs of neoangiogenesis cannot be detected. Objectives To examine the role of VEGF and its receptors in the impaired angiogenesis of SSc. Methods Skin pO2 was measured intradermally using the pO2 histograph in 13 patients with SSc and in 5 healthy controls. Cultured SSc and normal skin fibroblasts were exposed to hypoxia and analysed for VEGF mRNA by real-time PCR (TaqMan). Immunohistochemistry with anti-VEGF-Receptor-1 and anti-VEGF-Receptor-2 antibodies was performed on skin biopsies of SSc patients and healthy controls. Serum samples of 47 patients with SSc and 21 healthy controls were analysed for VEGF by ELISA and correlated with clinical parameters. Results PO2 values from involved skin of SSc patients (23,7 ± 2,1 mmHg) were significantly lower compared to healthy controls (33,6 ± 4,1 mmHg) and non-involved skin areas (37,8 ± 8,6 mmHg, p Conclusion Our results suggest a hypoxia mediated activation of the VEGF/VEGF-receptor axis in SSc. The correlation with clinical parameters indicate that elevated levels of VEGF are a feature of early disease stages and might be protective against the development of fingertip ulcers. Since the feasibility of a treatment with VEGF has just been approved in other ischaemic diseases, the application of VEGF may be a therapeutic option for the vascular insufficiency in SSc." @default.
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- W3103264823 date "2001-06-01" @default.
- W3103264823 modified "2023-10-17" @default.
- W3103264823 title "OP0125 Overexpression of vascular endothelial growth factor (vegf) and its receptors in systemic sclerosis (ssc): evidence for protective effects of vegf against the development of fingertip ulcers" @default.
- W3103264823 doi "https://doi.org/10.1136/annrheumdis-2001.299" @default.
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