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首页> 外文期刊>International Journal of Molecular Sciences >Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy
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Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy

机译：紫外线诱导的细胞凋亡的分子机制及其对皮肤驻留细胞的影响：基于紫外线的光疗的意义。

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The human skin is an integral system that acts as a physical and immunological barrier to outside pathogens, toxicants, and harmful irradiations. Environmental ultraviolet rays (UV) from the sun might potentially play a more active role in regulating several important biological responses in the context of global warming. UV rays first encounter the uppermost epidermal keratinocytes causing apoptosis. The molecular mechanisms of UV-induced apoptosis of keratinocytes include direct DNA damage (intrinsic), clustering of death receptors on the cell surface (extrinsic), and generation of ROS. When apoptotic keratinocytes are processed by adjacent immature Langerhans cells (LCs), the inappropriately activated Langerhans cells could result in immunosuppression. Furthermore, UV can deplete LCs in the epidermis and impair their migratory capacity, leading to their accumulation in the dermis. Intriguingly, receptor activator of NF-κB (RANK) activation of LCs by UV can induce the pro-survival and anti-apoptotic signals due to the upregulation of Bcl-xL, leading to the generation of regulatory T cells. Meanwhile, a physiological dosage of UV can also enhance melanocyte survival and melanogenesis. Analogous to its effect in keratinocytes, a therapeutic dosage of UV can induce cell cycle arrest, activate antioxidant and DNA repair enzymes, and induce apoptosis through translocation of the Bcl-2 family proteins in melanocytes to ensure genomic integrity and survival of melanocytes. Furthermore, UV can elicit the synthesis of vitamin D, an important molecule in calcium homeostasis of various types of skin cells contributing to DNA repair and immunomodulation. Taken together, the above-mentioned effects of UV on apoptosis and its related biological effects such as proliferation inhibition, melanin synthesis, and immunomodulations on skin residential cells have provided an integrated biochemical and molecular biological basis for phototherapy that has been widely used in the treatment of many dermatological diseases.
机译：人体皮肤是不可或缺的系统，对外界病原体，有毒物质和有害辐射具有物理和免疫屏障的作用。在全球变暖的背景下，来自太阳的环境紫外线（UV）可能在调节几种重要的生物反应中发挥更积极的作用。紫外线首先遇到最上层的表皮角质形成细胞，导致细胞凋亡。紫外线诱导的角质形成细胞凋亡的分子机制包括直接DNA损伤（内在），细胞表面死亡受体簇集（外在）和产生ROS。当邻近的未成熟朗格汉斯细胞（LC）处理凋亡的角质形成细胞时，激活不当的朗格汉斯细胞可能导致免疫抑制。此外，紫外线会耗尽表皮中的LC，并削弱其迁移能力，从而导致其在真皮中积累。有趣的是，由于Bcl-xL的上调，UV对LC的NF-κB（RANK）激活的受体激活剂可诱导促存活和抗凋亡信号，从而导致调节性T细胞的产生。同时，生理剂量的紫外线还可以增强黑色素细胞的存活和黑色素生成。与其在角质形成细胞中的作用相似，紫外线的治疗剂量可以通过黑素细胞中Bcl-2家族蛋白的移位来诱导细胞周期停滞，激活抗氧化剂和DNA修复酶并诱导凋亡，从而确保黑素细胞的基因组完整性和存活。此外，紫外线可以引发维生素D的合成，维生素D是各种类型皮肤细胞钙稳态中的重要分子，有助于DNA修复和免疫调节。综上所述，紫外线对细胞凋亡的上述作用及其相关的生物学作用，例如对皮肤驻留细胞的增殖抑制，黑色素合成和免疫调节，为光疗提供了综合的生化和分子生物学基础，已被广泛用于治疗许多皮肤病。

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