Kovacs Daniela, Raffa Salvatore, Flori Enrica, Aspite Nicaela, Briganti Stefania, Cardinali Giorgia, Torrisi Maria Rosaria, Picardo Mauro
Istituto Dermatologico San Gallicano, IRCCS, Via Elio Chianesi 53, 00144 Rome, Italy.
J Dermatol Sci. 2009 May;54(2):106-13. doi: 10.1016/j.jdermsci.2009.01.005. Epub 2009 Feb 27.
Exposure to ultraviolet (UV) radiation causes a complex cellular response, mostly mediated by the production of reactive oxygen species (ROS), which can be counteracted by exogenous treatments and endogenous mechanisms with anti-oxidant and scavenger properties. Keratinocyte growth factor (KGF/FGF7), a member of the fibroblast growth factor family, promotes epithelial growth and differentiation and is involved in cell survival after oxidant injuries.
We analyzed the role of KGF in the control of intracellular ROS production and oxidative stress after UVB exposure on KGF receptor (KGFR) transfected cells and human immortalized and primary keratinocytes.
We assessed the intracellular ROS production measuring the intensity of the oxidation-sensitive fluorescent probe 2',7'-dichlorofluorescein diacetate (DCFH-DA) by confocal microscopy, as well as the catalase activity by spectrophotometric assay. Moreover, morphological and biochemical analysis of actin cytoskeleton reorganization was evaluated as a further marker of oxidative damage.
Our data show that KGF significantly reduces intracellular ROS generation in response to UVB, preserves the decrease of catalase activity and prevents actin cytoskeleton rearrangement.
Our results provide a further evidence that KGF may be crucial for an efficient skin photoprotection, demonstrating a direct role for KGF in the reduction of intracellular ROS content following UVB exposure.
紫外线（UV）照射会引发复杂的细胞反应，主要由活性氧（ROS）的产生介导，而外源性治疗和具有抗氧化及清除剂特性的内源性机制可对抗这种反应。角质形成细胞生长因子（KGF/FGF7）是成纤维细胞生长因子家族的一员，可促进上皮细胞生长和分化，并参与氧化损伤后的细胞存活过程。
我们分析了KGF在紫外线B（UVB）照射后对转染KGF受体（KGFR）的细胞以及人永生化和原代角质形成细胞内ROS产生和氧化应激的控制作用。
我们通过共聚焦显微镜测量氧化敏感荧光探针2',7'-二氯荧光素二乙酸酯（DCFH-DA）的强度来评估细胞内ROS的产生，并通过分光光度法测定过氧化氢酶活性。此外，对肌动蛋白细胞骨架重组进行形态学和生化分析，将其作为氧化损伤的进一步标志物进行评估。
我们的数据表明，KGF可显著减少UVB诱导的细胞内ROS生成，维持过氧化氢酶活性的降低，并防止肌动蛋白细胞骨架重排。
我们的结果进一步证明KGF可能对有效的皮肤光保护至关重要，表明KGF在UVB照射后降低细胞内ROS含量方面具有直接作用。
