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首页> 外文期刊>Journal of Photochemistry and Photobiology, B. Biology: Official Journal of the European Society for Photobiology >Low doses of ultraviolet A radiation stimulate adhesion of human dermal fibroblasts by integrins in a protein kinase C-dependent pathway
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Low doses of ultraviolet A radiation stimulate adhesion of human dermal fibroblasts by integrins in a protein kinase C-dependent pathway

机译:低剂量的紫外线A辐射通过蛋白激酶C依赖性途径中的整合素刺激人皮肤成纤维细胞的粘附

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In this work, we have studied the modulation of fibroblast-extracellular matrix interactions by physiological doses of ultraviolet A (UV-A) radiation using an adhesion assay on collagen. We have shown that low doses of UV-A (20 kJ/m~2) stimulate fibroblast adhesion while higher doses (100 and 200 kJ/m~2) inhibit it. By measurement of the thiobarbituric acid reactive substances (TBARS) and use of the chain-breaking antioxidant vitamin E, no role of lipid peroxidation can be detected in these effects. By incubating fibroblasts with a specific protein kinase C (PKC) inhibitor, GF109203X, we have demonstrated that the stimulation of the adhesion by low doses of UV-A involves, at least in part, a PKC-dependent mechanism. In addition, using function-blocking antibodies of #alpha#1, #alpha#2 or #alpha#5 integrin chains involved in extracellular matrix anchorage, we have shown that they decrease the stimulation of adhesion following low doses of UV-A radiation, demonstrating the involvement of these three integrin chains in this UV-A effect. In parallel, 20 kJ/m~2 of UV-A are found to rapidly stimulate membrane expression of #alpha#1, #alpha#2 and #alpha#5 integrin chains. This work, which underlines the involvement of integrins in UV-A effects, contributes to the evaluation of the mechanisms by which cell-matrix interactions modulate cell behaviour.
机译:在这项工作中,我们研究了使用胶原蛋白的粘附测定法通过生理剂量的紫外线A(UV-A)辐射对成纤维细胞与细胞外基质相互作用的调节。我们发现低剂量的UV-A(20 kJ / m〜2)刺激成纤维细胞粘附,而高剂量的UV-A(100和200 kJ / m〜2)抑制它。通过测量硫代巴比妥酸反应性物质(TBARS)和使用链断裂抗氧化剂维生素E,无法在这些作用中检测到脂质过氧化作用。通过将成纤维细胞与特定的蛋白激酶C(PKC)抑制剂GF109203X孵育,我们证明了低剂量的UV-A刺激粘连至少部分涉及PKC依赖性机制。此外,使用参与细胞外基质锚定的#alpha#1,#alpha#2或#alpha#5整联蛋白链的功能阻断抗体,我们发现它们可降低低剂量的UV-A辐射后对粘连的刺激,证明这三个整合素链参与了这种UV-A效应。同时,发现20 kJ / m〜2的UV-A可以迅速刺激#alpha#1,#alpha#2和#alpha#5整联蛋白链的膜表达。这项工作强调了整联蛋白在UV-A效应中的参与,有助于评估细胞基质相互作用调节细胞行为的机制。

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