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Examination of Bcl‐2, Bcl‐X and bax protein expression in psoriasis
Author(s) -
Koçak Mukadder,
Bozdoǧan Önder,
Erkek Emel,
Atasoy Pínar,
Birol Ahu
Publication year - 2003
Publication title -
international journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.677
H-Index - 93
eISSN - 1365-4632
pISSN - 0011-9059
DOI - 10.1046/j.1365-4362.2003.01821.x
Subject(s) - psoriasis , epidermis (zoology) , apoptosis , immunohistochemistry , pathogenesis , bcl 2 associated x protein , pathology , cancer research , keratinocyte , medicine , biology , immunology , programmed cell death , in vitro , caspase 3 , biochemistry , anatomy
Background Psoriasis is an inflammatory skin disease characterized by epidermal hyperplasia and greatly accelerated epidermal turnover. The blockage of normal apoptotic process in the epidermis is one of the factors implicated in the pathogenesis of psoriasis. Objective The purpose of the present study was to elucidate whether bcl‐family proteins are significantly involved in the hypothetical antiapoptotic cascade in lesional psoriatic epidermis. Methods Twenty‐six lesional biopsy samples of 26 patients with psoriasis and five control specimens from normal skin were studied by immunohistochemical method for the differential expression of pro‐apoptotic bax and antiapoptotic bcl‐2 and bcl‐x proteins. Results Compared with the normal epidermis, bcl‐2 expression was significantly reduced, whereas bax and bcl‐x were significantly overexpressed in the psoriatic epidermis. The localization of bcl‐2/bax/bcl‐x proteins in the psoriatic epidermis did not show a significant deviation from that in the normal epidermis. Conclusion These findings indicate a discordant expression of bcl‐2 and bax/bcl‐x in psoriatic epidermis. Increased bcl‐x expression might contribute to the antiapoptotic response in psoriatic keratinocytes. The presence of strong bax expression with a concomitant decrease in bcl‐2 expression suggests either a functional defect in bax protein or an inherent/acquired resistance to bax‐mediated apoptosis in psoriatic keratinocytes.