细胞衰老的特征是细胞周期停滞和衰老相关分泌表型 (SASP),可由多种刺激触发,包括脱氧核糖核酸 (DNA) 损伤、氧化应激和端粒耗竭。细胞衰老与皮肤老化有关,识别衰老细胞的特异性标志物对于开发靶向疗法至关重要。组织蛋白酶 F (CTSF) 与皮炎和各种癌症有关,并通过与 Bcl 家族蛋白的结合参与细胞永生化。特异性标记和清除因衰老永生化的人体皮肤成纤维细胞和角质形成细胞,实现嫩肤的候选治疗靶点。在这项研究中,我们调查了 CTSF 是否与人成纤维细胞和角质形成细胞的衰老有关。在使用复制老化、电离辐射暴露和抗癌药物多柔比星创建的衰老模型中,观察到各种衰老标记,例如衰老相关 β-半乳糖苷酶 (SA-β-gal) 活性、SASP 基因表达增加和摄取减少增殖标记 BrdU。此外,CTSF 表达在基因和蛋白质水平上升高。此外,CTSF 阳性细胞在老年人表皮和真皮的某些部分中很丰富。在分裂停滞的衰老细胞群中,CTSF 阳性细胞的数量明显高于增殖细胞群。这些结果表明 CTSF 是针对老化成纤维细胞和角质形成细胞的治疗方式的候选者。电离辐射暴露和抗癌药物多柔比星观察到各种衰老标志物,例如衰老相关 β-半乳糖苷酶 (SA-β-gal) 活性、SASP 基因表达增加和增殖标志物 BrdU 摄取减少。此外,CTSF 表达在基因和蛋白质水平上升高。此外,CTSF 阳性细胞在老年人表皮和真皮的某些部分中很丰富。在分裂停滞的衰老细胞群中,CTSF 阳性细胞的数量明显高于增殖细胞群。这些结果表明 CTSF 是针对老化成纤维细胞和角质形成细胞的治疗方式的候选者。电离辐射暴露和抗癌药物多柔比星观察到各种衰老标志物,例如衰老相关 β-半乳糖苷酶 (SA-β-gal) 活性、SASP 基因表达增加和增殖标志物 BrdU 摄取减少。此外,CTSF 表达在基因和蛋白质水平上升高。此外,CTSF 阳性细胞在老年人表皮和真皮的某些部分中很丰富。在分裂停滞的衰老细胞群中,CTSF 阳性细胞的数量明显高于增殖细胞群。这些结果表明 CTSF 是针对老化成纤维细胞和角质形成细胞的治疗方式的候选者。例如衰老相关的 β-半乳糖苷酶 (SA-β-gal) 活性、SASP 基因表达增加以及增殖标记 BrdU 的摄取减少。此外,CTSF 表达在基因和蛋白质水平上升高。此外,CTSF 阳性细胞在老年人表皮和真皮的某些部分中很丰富。在分裂停滞的衰老细胞群中,CTSF 阳性细胞的数量明显高于增殖细胞群。这些结果表明 CTSF 是针对老化成纤维细胞和角质形成细胞的治疗方式的候选者。例如衰老相关的 β-半乳糖苷酶 (SA-β-gal) 活性、SASP 基因表达增加以及增殖标记 BrdU 的摄取减少。此外,CTSF 表达在基因和蛋白质水平上升高。此外,CTSF 阳性细胞在老年人表皮和真皮的某些部分中很丰富。在分裂停滞的衰老细胞群中,CTSF 阳性细胞的数量明显高于增殖细胞群。这些结果表明 CTSF 是针对老化成纤维细胞和角质形成细胞的治疗方式的候选者。CTSF 阳性细胞大量存在于老年人表皮和真皮的某些部位。在分裂停滞的衰老细胞群中,CTSF 阳性细胞的数量明显高于增殖细胞群。这些结果表明 CTSF 是针对老化成纤维细胞和角质形成细胞的治疗方式的候选者。CTSF 阳性细胞大量存在于老年人表皮和真皮的某些部位。在分裂停滞的衰老细胞群中,CTSF 阳性细胞的数量明显高于增殖细胞群。这些结果表明 CTSF 是针对老化成纤维细胞和角质形成细胞的治疗方式的候选者。
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Cathepsin F is a potential marker for senescent human skin fibroblasts and keratinocytes associated with skin aging
Cellular senescence is characterized by cell cycle arrest and the senescence-associated secretory phenotype (SASP) and can be triggered by a variety of stimuli, including deoxyribonucleic acid (DNA) damage, oxidative stress, and telomere exhaustion. Cellular senescence is associated with skin aging, and identification of specific markers of senescent cells is essential for development of targeted therapies. Cathepsin F (CTSF) has been implicated in dermatitis and various cancers and participates in cell immortalization through its association with Bcl family proteins. It is a candidate therapeutic target to specifically label and eliminate human skin fibroblasts and keratinocytes immortalized by aging and achieve skin rejuvenation. In this study, we investigated whether CTSF is associated with senescence in human fibroblasts and keratinocytes. In senescence models, created using replicative aging, ionizing radiation exposure, and the anticancer drug doxorubicin, various senescence markers were observed, such as senescence-associated β-galactosidase (SA-β-gal) activity, increased SASP gene expression, and decreased uptake of the proliferation marker BrdU. Furthermore, CTSF expression was elevated at the gene and protein levels. In addition, CTSF-positive cells were abundant in aged human epidermis and in some parts of the dermis. In the population of senescent cells with arrested division, the number of CTSF-positive cells was significantly higher than that in the proliferating cell population. These results suggest that CTSF is a candidate for therapeutic modalities targeting aging fibroblasts and keratinocytes.