Bang B, Rygaard J, Baadsgaard O, Skov L
Department of Dermatology K/A 1502, Gentofte Hospital, University of Copenhagen, Niels Andersens Vej 65, 2900 Hellerup, Denmark.
Br J Dermatol. 2002 Dec;147(6):1199-206. doi: 10.1046/j.1365-2133.2002.04787.x.
Apoptosis has been proposed to act as an important mechanism for eliminating keratinocytes that have been irreversibly damaged by ultraviolet (UV) irradiation. One way to induce apoptosis in keratinocytes is through activation of the cell surface receptor Fas (CD95), either with the ligand (FasL) or directly with UV radiation.
To investigate the regulation of Fas and FasL expression in human skin and the formation of apoptotic cells after in vivo exposure to UVB or long-wave UVA radiation.
Volunteers were irradiated with either 3 minimal erythema doses (MED) of UVB (n = 6) or 3 MED of long-wave UVA (n = 6) on buttock skin 12, 24 and 72 h before skin punch biopsies were taken. Expression of Fas and FasL was demonstrated by immunohistochemistry on cryostat sections. Apoptosis was assessed by the terminal deoxynucleotidyl transferase-mediated fluorescein-deoxyuridine triphosphate nick-end labelling reaction.
In five of six subjects, exposure to UVB radiation resulted in increased homogeneous expression of Fas on epidermal cells, with greatest expression at 24 and 72 h after irradiation. In all subjects, exposure to long-wave UVA resulted in increased homogeneous expression of Fas on epidermal cells, with greatest expression at 12 h after irradiation. In five of six subjects, exposure to UVB radiation resulted in temporarily decreased expression of FasL, but after 72 h the expression of FasL had returned to the preirradiation level. The expression of FasL on epidermal cells after exposure to long-wave UVA showed considerable variation. UVB irradiation was a stronger inducer of epidermal apoptosis than was UVA irradiation. The number of apoptotic epidermal cells did not correlate with expression of Fas or FasL.
In human skin the expression of Fas on epidermal cells increases after in vivo exposure to UVB or long-wave UVA. Exposure to UVB causes a temporary decrease in the expression of FasL on epidermal cells.
细胞凋亡被认为是清除因紫外线（UV）照射而受到不可逆损伤的角质形成细胞的重要机制。诱导角质形成细胞凋亡的一种方法是通过激活细胞表面受体Fas（CD95），可使用配体（FasL）或直接用紫外线辐射。
研究人体皮肤中Fas和FasL表达的调节以及体内暴露于中波紫外线（UVB）或长波紫外线（UVA）辐射后凋亡细胞的形成。
在进行皮肤打孔活检前12、24和72小时，对志愿者臀部皮肤照射3个最小红斑量（MED）的UVB（n = 6）或3个MED的长波UVA（n = 6）。通过免疫组织化学在低温恒温器切片上检测Fas和FasL的表达。通过末端脱氧核苷酸转移酶介导的荧光素-脱氧尿苷三磷酸缺口末端标记反应评估细胞凋亡。
在六名受试者中的五名中，UVB辐射导致表皮细胞上Fas表达均匀增加，在照射后24和72小时表达最高。在所有受试者中，长波UVA辐射导致表皮细胞上Fas表达均匀增加，在照射后12小时表达最高。在六名受试者中的五名中，UVB辐射导致FasL表达暂时降低，但72小时后FasL表达恢复到照射前水平。长波UVA照射后表皮细胞上FasL的表达有很大差异。UVB照射比UVA照射更能诱导表皮细胞凋亡。凋亡表皮细胞的数量与Fas或FasL的表达无关。
在人体皮肤中，体内暴露于UVB或长波UVA后，表皮细胞上Fas的表达增加。暴露于UVB会导致表皮细胞上FasL的表达暂时降低。
