Expression pattern of the bcl-2 homologous protein bad in normal skin, psoriasis vulgaris and keratinocytic tumors

• Published in: Journal of dermatological science 2000-02, Vol.22 (2), p.132-137
• Main Authors: Tomková, Hana, Fujimoto, Wataru, Arata, Jirô
• Format: Article
• Language: English
• Subjects: Apoptosis; Bad; bcl-2 family; bcl-Associated Death Protein; Carrier Proteins - biosynthesis; Cell Death; Humans; Keratinocytes - metabolism; Keratinocytes - pathology; Non-melanoma skin cancer; Proto-Oncogene Proteins c-bcl-2 - metabolism; Psoriasis - metabolism; Psoriasis - pathology; Psoriasis vulgaris; Skin - metabolism; Skin - pathology; Skin disease; Skin Neoplasms - metabolism; Skin Neoplasms - pathology
• ISSN: 0923-1811; 1873-569X
• DOI: 10.1016/S0923-1811(99)00058-4

Previous investigations focused on the mechanisms and regulation of apoptotic process have found that bcl-2 and its homologous proteins are central regulators of the mitochondrial phase of apoptosis. Expression of several members of the bcl-2 family has been studied in various tissues including skin under normal as well as disease conditions. In this report, we investigated the expression of bad, the pro-apoptotic member of the BH3 subfamily, in normal and psoriatic epidermis, keratoacanthoma, and basal and squamous cell carcinomas. Normal and psoriatic epidermis showed accentuation of the staining in the lower suprabasal compartment. A weak, predominantly diffuse staining pattern was observed in the upper epidermis of psoriatic plaques. Keratoacanthoma showed strong but diffuse immunostaining for pro-apoptotic bad, however we found only weak bad expression in squamous cell carcinoma. Seven out of 15 basal cell carcinomas failed to express bad protein. There was no correlation between bad positivity and depth of tumour infiltration. Our observation suggests that the pro-apoptotic bad may function as one of regulators involved in the maintenance of epidermal homeostasis and this function could be altered depending on the disease state.