HSP27 Protects Skin From Ultraviolet B -Induced Photodamage by Regulating Autophagy and Reactive Oxygen Species Production.
HSP27 Protects Skin From Ultraviolet B -Induced Photodamage by Regulating Autophagy and Reactive Oxygen Species Production.
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HSP27 通过调节自噬和活性氧物质的产生来保护皮肤免受紫外线 B 引起的光损伤
DOI：
10.3389/fcell.2022.852244
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发表时间：
2022
影响因子：
5.5
通讯作者：
中科院分区：
文献类型：
--
作者：
紫外线(UV)照射已被证明与我们所知的几乎所有皮肤问题有关，真皮和表皮都可能不同程度地受到紫外线照射的影响。每次在没有防护的情况下暴露在阳光下，我们的皮肤都会更接近光老化，最终导致不可逆转的后果。热休克蛋白27(HSP27)是参与细胞生长、自噬、细胞凋亡、耐药、肿瘤发生和转移的重要蛋白。有证据表明，生物体受到各种内外部环境应激(热、氧化应激、有机毒物等)的影响，高表达的HSP27具有保护作用。然而，HSP27在应对紫外线照射中的表达还没有得到彻底的研究。本研究通过不同剂量的UVB照射人表皮角质形成细胞(HEKs)(30nmJ/cm2)、人真皮成纤维细胞(HDFS)(150mJ/cm2)和小鼠皮肤(2700mJ/cm2)，建立光损伤模型。Hsp27基因敲除降低了细胞存活率，增加了UVB诱导的活性氧(ROS)的产生。我们在体内和体外都得到了一致的结果。与UVB组相比，UVB+si-HSP27组LC3B的表达显著降低，而p62的表达显著升高。HSP27基因敲除后，细胞内超氧化物歧化酶(SOD)和过氧化氢酶(CAT)等抗氧化剂的表达减少，从而加速了UVB诱导的ROS释放。组织学结果显示，UVB+si-HSP27组表皮增厚，胶原纤维排列紊乱。这些发现表明，HSP27可能通过维持正常的自噬和抗氧化水平，在UVB诱导的皮肤损伤过程中发挥光保护作用。提示HSP27可能是光损伤的潜在治疗靶点。然而，确定最终的机制还需要进一步的探索。
Ultraviolet (UV) irradiation has been well documented to be linked with almost all skin problems we know, and both dermis and epidermis may be affected to varying degrees by UV irradiation. Every time when exposed to sunlight without protection, our skin will step closer to photoaging, leading to irreversible consequences ultimately. Heat shock protein 27 (HSP27) is a vital protein involved in cell growth, autophagy, apoptosis, drug resistance, tumor genesis and metastasis. Evidence suggests that the organism is subjected to various internal and external environmental stresses (heat, oxidative stress, organic toxicants, etc.), and HSP27 with high expression has protective function. However, the expression of HSP27 in coping with UV irradiation have not been examined thoroughly. In this study, photodamage models were developed through different doses of UVB irradiation in human epidermal keratinocytes (HEKs) (30 mJ/cm2), human dermal fibroblasts (HDFs) (150 mJ/cm2) and mouse skin (2,700 mJ/cm2). HSP27 knockdown decreased cell viability and increased the incidence of UVB-induced reactive oxygen species (ROS) production. We got consistent results in vivo and vitro. Compared with that in the UVB group, the expression of LC3B was significantly lower, while the expression of p62 was significantly higher in the UVB + si-HSP27 group. It was also revealed that HSP27 knockdown reduced the expressions of some antioxidants, such as superoxide dismutase (SOD) and catalase (CAT), which accelerated UVB-induced ROS release. Moreover, histological results showed that epidermis was thickened and collagen fibers were disorganized in the UVB + si-HSP27 group. These findings have demonstrated that HSP27 might play a photoprotective role in the UVB-induced skin damage process by maintaining the normal autophagy and antioxidant level. It is implied that HSP27 could be a potential therapeutic target of photodamage. However, determination of the definitive mechanism requires further exploration.
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