Staff Publications

Staff Publications

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    'Staff publications' is the digital repository of Wageningen University & Research

    'Staff publications' contains references to publications authored by Wageningen University staff from 1976 onward.

    Publications authored by the staff of the Research Institutes are available from 1995 onwards.

    Full text documents are added when available. The database is updated daily and currently holds about 240,000 items, of which 72,000 in open access.

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    We will mail you new results for this query: keywords==human keratinocytes
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UVA1 radiation inhibits calcineurin through oxidative damage mediated by photosensitization
Musson, R.E.A. ; Hensbergen, P.J. ; Westphal, A.H. ; Temmink, W.P.M. ; Deelder, A.M. ; Pelt, J. van; Mullenders, L.H.F. ; Smit, N.P.M. - \ 2011
Free Radical Biology and Medicine 50 (2011)10. - ISSN 0891-5849 - p. 1392 - 1399.
singlet molecular-oxygen - light-emission measurements - transcription factor nfat - human skin fibroblasts - kappa-b activity - hydrogen-peroxide - cyclosporine-a - ultraviolet-radiation - phosphatase-activity - human keratinocytes
The protein phosphatase calcineurin has been gradually revealing itself as the central controller of our immune response, although it is involved in a wide array of signaling pathways related to cellular development and cell cycle progression. As such, calcineurin is an attractive, yet delicate, therapeutic target for the prevention of allograft rejection and treatment of several inflammatory skin conditions. However, calcineurin activity is not only sensitive to immunosuppressants such as cyclosporin A and tacrolimus, but also subject to modulation by reactive oxygen species. We have recently shown, both in vivo and in vitro, that UVA1 radiation suppresses calcineurin activity. In this paper, we present evidence that this activity loss is due to singlet oxygen and superoxide generated by photosensitization and show that a closely related phosphatase, PP2A, is not affected. Furthermore, a survey of this damage reveals oxidation of several Met and Cys residues as well as an overall conformational change. These findings provide a mechanistic basis for the hypothesis that UVA1 and calcineurin inhibitors both affect the same signal transduction pathway in skin.
Enzymatically-tailored pectins differentially influence the morphology, adhesion, cell cycle progression and survival of fibroblasts
Nagel, M.D. ; Verhoef, R.P. ; Schols, H.A. ; Morra, M. ; Knox, J.P. ; Ceccone, G. ; Volpe, C.D. ; Vigneron, P. ; Bussy, C. ; Gallet, M. ; Velzenberger, E. ; Vayssade, M. ; Cascardo, G. ; Cassinelli, C. ; Haeger, A. ; Gilliland, D. ; Liakos, I. ; Rodrigues-Valverde, M. ; Siboni, S. - \ 2008
Biochimica et Biophysica Acta. General subjects 1780 (2008)7-8. - ISSN 0304-4165 - p. 995 - 1003.
hairy ramified regions - growth-factor receptors - surface-chemistry - fibronectin conformation - arabinogalactan-proteins - monoclonal-antibodies - human keratinocytes - integrin binding - adsorbed fibronectin - rhamnogalacturonan-i
Improved biocompatibility and performance of biomedical devices can be achieved through the incorporation of bioactive molecules on device surfaces. Five structurally distinct pectic polysaccharides (modified hairy regions (MHRs)) were obtained by enzymatic liquefaction of apple (MHR-B, MHR-A and MHR-), carrot (MHR-C) and potato (MHR-P) cells. Polystyrene (PS) Petri dishes, aminated by a plasma deposition process, were surface modified by the covalent linking of the MHRs. Results clearly demonstrate that MHR-B induces cell adhesion, proliferation and survival, in contrast to the other MHRs. Moreover, MHR- causes cells to aggregate, decrease proliferation and enter into apoptosis. Cells cultured in standard conditions with 1% soluble MHR-B or MHR- show the opposite behaviour to the one observed on MHR-B and --grafted PS. Fibronectin was similarly adsorbed onto MHR-B and tissue culture polystyrene (TCPS) control, but poorly on MHR-. The Fn cell binding site (RGD sequence) was more accessible on MHR-B than on TCPS control, but poorly on MHR-. The disintegrin echistatin inhibited fibroblast adhesion and spreading on MHR-B-grafted PS, which suggests that MHRs control fibroblast behaviour via serum-adhesive proteins. This study provides a basis for the design of intelligently-tailored biomaterial coatings able to induce specific cell functions.
IL-23 promotes CD4(+) T cells to produce IL-17 in Vogt-Koyanagi-Harada disease
Chi, W. ; Yang, P.Z. ; Li, B. ; Wu, C.Y. ; Jin, H.L. ; Zhu, X.F. ; Chen, L.N. ; Zhou, H.Y. ; Huang, X.K. ; Kijlstra, A. - \ 2007
Journal of Allergy and Clinical Immunology 119 (2007)5. - ISSN 0091-6749 - p. 1218 - 1224.
proinflammatory cytokine production - autoimmune inflammation - sympathetic ophthalmia - rheumatoid-arthritis - human keratinocytes - interferon-gamma - interleukin-17 - expression - lymphocytes - distinct
Background: Vogt-Koyanagi-Harada (VKH) disease is a systemic refractory autoimmune disease. IL-23 has been thought to play a critical role in autoimmune disease through inducing the development of IL-17-producing CD4(+) T cells. Objective: To investigate the expression of IL-23 and IL-17 and the influence of IL-23 on IL-17 production in patients with VKH disease. Methods: Blood samples were taken from 25 patients with VKH disease and 16 healthy controls. Peripheral blood mononuclear cells (PBMCs) were subjected to analysis of IL-23p19 mRNA and IL-23 protein expression using RT-PCR and ELISA, respectively. The IL-17 levels in the supernatants of PBMCs and CD4(+) T cells cultured in the absence or presence of recombinant (r)IL-23, rIL-12, or anti-IFN-gamma were determined by ELISA. Results: The patients with VKH disease with active uveitis showed an elevated level of IL-23p19 mRNA in PBMCs, higher IL-23 in the serum and supernatants of PBMCs, and increased production of IL-17 by polyclonally stimulated PBMCs and CD4+ T cells. Recombinant IL-23 significantly enhanced IL-17 production, whereas rIL-12 and IFN-gamma inhibited IL-17 production. More importantly, IL-17 production was significantly increased in patients with active uveitis in the presence of rIL-23. Both rIL-23 and rIL-12 enhanced IFN-gamma production. Conclusion: The results suggest that IL-23-stimulated production of IL-17 by CD4+ T cells may be responsible for the development of uveitis seen in patients with VKH disease. Clinical implications: This study provides a new insight into the mechanism involved in the development of VKH disease.
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