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首页> 外文期刊>Journal of dermatological science >Oxidative stress mediated Ca2+ release manifests endoplasmic reticulum stress leading to unfolded protein response in UV-B irradiated human skin cells
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Oxidative stress mediated Ca2+ release manifests endoplasmic reticulum stress leading to unfolded protein response in UV-B irradiated human skin cells

机译：氧化应激介导的Ca2 +释放表现出内质网应激，导致UV-B照射的人皮肤细胞中蛋白反应展开

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摘要

Background: Exposure of skin to ultraviolet (UV) radiation, an environmental stressor induces number of adverse biological effects (photodamage), including cancer. The damage induced by UV-irradiation in skin cells is initiated by the photochemical generation of reactive oxygen species (ROS) and induction of endoplasmic reticulum (ER) stress and consequent activation of unfolded protein response (UPR). Objective: To decipher cellular and molecular events responsible for UV-B mediated ER stress and UPR activation in skin cells. Methods: The study was performed on human skin fibroblast (Hs68) and keratinocyte (HaCaT) cells exposed to UV-B radiations in lab conditions. Different parameters of UVB induced cellular and molecular changes were analyzed using Western-blotting, microscopic studies and flow cytometry. Results: Our results depicted that UV-B induces an immediate ROS generation that resulted in emptying of ER Ca2+ stores inducing ER stress and activation of PERK-peIF2α-CHOP pathway. Quenching ROS generation by anti-oxidants prevented Ca2+ release and subsequent induction of ER stress and UPR activation. UV-B irradiation induced PERK dependent G2/M phase cell cycle arrest in Hs68 and G1/S phase cell cycle arrest in HaCaT. Also our study reflects that UV-B exposure leads to loss of mitochondrial membrane potential, activation of apoptotic cascade as evident by AnnexinV/PI staining, decreased expression of Bcl-2 and increased cleavage of PARP-1 protein. Conclusion: UV-B induced Ca2+ deficit within ER lumen was mediated by immediate ROS generation. Insufficient Ca2+ concentration within ER lumen developed ER stress leading to UPR activation. These changes were reversed by use of anti-oxidants which quench ROS.
机译：背景：皮肤暴露于紫外线（UV）辐射下，环境压力会引起许多不利的生物学效应（光损伤），包括癌症。紫外线照射引起的皮肤细胞损伤是由光化学活性氧（ROS）的产生，内质网（ER）应力的诱导以及未折叠蛋白应答（UPR）的激活引起的。目的：解释负责皮肤细胞中UV-B介导的ER应激和UPR活化的细胞和分子事件。方法：在实验室条件下，对暴露于UV-B辐射的人皮肤成纤维细胞（Hs68）和角质形成细胞（HaCaT）细胞进行了研究。使用蛋白质印迹，显微镜研究和流式细胞仪分析了UVB诱导的细胞和分子变化的不同参数。结果：我们的结果表明，UV-B诱导立即产生ROS，从而导致ER Ca2 +存储库排空，从而诱导ER应激并激活PERK-peIF2α-CHOP途径。通过抗氧化剂淬灭ROS可以防止Ca2 +释放以及随后诱导的ER应激和UPR激活。 UV-B辐射诱导Hs68中PERK依赖的G2 / M期细胞周期停滞和HaCaT中G1 / S期细胞周期停滞。我们的研究还表明，UV-B暴露会导致线粒体膜电位的丧失，膜联蛋白V / PI染色所证实的凋亡级联反应的激活，Bcl-2表达的降低以及PARP-1蛋白的裂解增加。结论：UV-B诱导的内腔内Ca2 +缺乏症是由立即产生的ROS介导的。 ER腔内Ca2 +浓度不足会产生ER应力，从而导致UPR激活。这些变化可以通过使用抗氧化剂来逆转ROS来逆转。

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