Gilhar A, Ullmann Y, Karry R, Shalaginov R, Assy B, Serafimovich S, Kalish R S
Skin Research Laboratory, Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Br J Dermatol. 2004 Jan;150(1):56-63. doi: 10.1111/j.1365-2133.2004.05715.x.
Aged human epidermis is characterized by morphological changes including flattening of the dermal-epidermal junction and a decrease in thickness.
To determine the roles of proliferation, apoptosis, Fas (CD95), Fas ligand (FasL) and telomerase in changes of human epidermis during ageing.
Human epidermis from aged subjects (n = 14; mean age 70.7 years) and young subjects (n = 14; mean age 23.4 years) was studied by histology, immunohistochemistry, terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labelling assay for apoptotic cells and reverse transcription-polymerase chain reaction to determine epidermal thickness, proliferation (Ki-67), apoptosis, expression of Fas and FasL, and telomerase activity.
Aged skin was associated with thinning of the epidermis, decreased proliferation, and increased apoptosis below the granular layer. This was associated with increased epidermal expression of Fas and FasL. Telomerase activity was similar in aged and young epidermis.
Fas/FasL-mediated apoptosis, along with decreased proliferation, may have a role in changes of human epidermis during ageing. Telomerase activity did not appear to be limiting in young vs. old human epidermis.
衰老的人类表皮具有形态学变化特征,包括真皮 - 表皮连接处变平以及厚度减小。
确定增殖、凋亡、Fas(CD95)、Fas配体(FasL)和端粒酶在人类表皮衰老过程变化中的作用。
通过组织学、免疫组织化学、用于凋亡细胞的末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸缺口末端标记法以及逆转录 - 聚合酶链反应,研究老年受试者(n = 14;平均年龄70.7岁)和年轻受试者(n = 14;平均年龄23.4岁)的人类表皮,以确定表皮厚度、增殖(Ki - 67)、凋亡、Fas和FasL的表达以及端粒酶活性。
老年皮肤与表皮变薄、增殖减少以及颗粒层以下凋亡增加有关。这与表皮Fas和FasL表达增加有关。老年和年轻表皮中的端粒酶活性相似。
Fas/FasL介导的凋亡以及增殖减少可能在人类表皮衰老过程变化中起作用。端粒酶活性在年轻与老年人类表皮中似乎没有限制作用。