The expression of retinoblastoma protein in epidermis is induced by ultraviolet B exposure.
DNA damage induced by ultraviolet light (UV) can be repaired while cells are arrested in the cell cycle. Tumour suppressor gene p53 has been implicated as being involved in the G1 arrest after UV irradiation. Normal human skin from three volunteers was exposed to UVB and the expression of p53, Ki-67 and retinoblastoma gene product (pRb) was examined immunohistochemically, in addition to observation for sunburn cells. p53 protein started to be expressed at 6 h after UVB irradiation. It peaked at 12-48 h. Ki-67 expression was induced after 48 or 72 h of irradiation. pRb begun to be expressed at 24 or 48 h and peaked at 48-96 h. p53-positive cells were distributed throughout the epidermis, while Ki-67 and pRb positive cells were seen mainly at the lower epidermis. Finally, sunburn cells, which are presumably apoptotic cells, appeared at 24 h and peaked at 24-48 h and were seen at upper epidermis. The different and co-ordinated expression, although variable between individuals, indicates important roles for p53 and pRb on the maintenance of the homeostasis of the epidermis after UV irradiation.
Ueda
M
M
Department of Dermatology, Kobe University School of Medicine, Japan.
Ahmed
N U
NU
Bito
T
T
Nagano
T
T
Ichihashi
M
M
D004817:Epidermis / Q000378:metabolism* / Q000528:radiation effects*; D006801:Humans; D007124:Immunoenzyme Techniques; D019394:Ki-67 Antigen / Q000096:biosynthesis; D016160:Retinoblastoma Protein / Q000096:biosynthesis*; D013471:Sunburn / Q000378:metabolism / Q000473:pathology; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis; D014466:Ultraviolet Rays
D019394:Ki-67 Antigen; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53