Wounding with a microneedling device corrects the inappropriate ultraviolet B radiation response in geriatric skin.
Wounding with a microneedling device corrects the inappropriate ultraviolet B radiation response in geriatric skin.
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使用微针装置进行创伤可纠正老年皮肤不适当的紫外线 B 辐射反应。
DOI：
10.1007/s00403-019-02001-z
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发表时间：
2020
影响因子：
3
通讯作者：
Spandau,DanF
中科院分区：
文献类型：
--
作者：
Travers,JeffreyB;Kemp,MichaelG;Weir,NathanM;Cates,Elizabeth;Alkawar,AbdulrahmanM;Mahajan,AvinashS;Spandau,DanF
非黑色素瘤皮肤癌主要影响老年患者，这一事实证明，这些癌症中只有20%是在60岁以下的患者中诊断出来的。重要的是，老年皮肤对致癌紫外线B辐射（UVB）的反应方式允许肿瘤细胞的建立。最近的研究已经表明，用分次换肤激光和磨皮术对老年人皮肤的创伤上调成纤维细胞产生胰岛素样生长因子-1（IGF-1），并使由基底角质形成细胞增殖组成的前致癌急性UVB反应正常化，同时仍具有未修复的DNA损伤。本研究测试了用市售微针装置创伤以上调IGF-1水平并使老年UVB反应正常化的能力。老年志愿者用微针装置在受损皮肤上进行治疗，3个月后，在受伤皮肤与对照皮肤中测试IGF-1水平和UVB反应。通过微针的创伤上调IGF-1，并导致较低水平的基底角质形成细胞增殖与未修复的DNA损伤。微针保护免受UVB损伤的增殖性角质形成细胞形成的能力表明这种创伤方式减少衰老相关的非黑色素瘤皮肤癌的潜力。
Non-melanoma skin cancer primarily affects geriatric patients as evidenced by the fact that only 20% of these cancers are diagnosed in patients under the age of 60 years. Of importance, geriatric skin responds to procarcinogenic ultraviolet B radiation (UVB) in a manner that permits the establishment of tumor cells. Recent studies have indicated that wounding of geriatric skin with fractionated resurfacing lasers and dermabrasion upregulates fibroblast production of insulin-like growth factor-1 (IGF-1) and normalizes the procarcinogenic acute UVB response consisting of basal keratinocytes proliferating while still harboring unrepaired DNA damage. The present studies tested the ability of wounding with a commercially available microneedling device to upregulate IGF-1 levels and normalize the geriatric UVB response. Geriatric volunteers were treated with a microneedling device on buttock skin and 3 months later the IGF-1 levels and UVB responses tested in wounded vs control skin. Wounding via microneedling upregulated IGF-1 and resulted in lower levels of basal keratinocytes proliferating with unrepaired DNA damage. The ability of microneedling to protect against the formation of UVB-damaged proliferating keratinocytes indicates the potential of this wounding modality to reduce aging-associated non-melanoma skin cancer.