Expression Of Bciz And p53 In Psoriasis

Abstract

Psoriasis is a common benign hyperproliferative disorder of the skin. Real "trigger" mechanism of basic etiopathogenesis occurring at the onset of the disease still remain unclear, even though it is demonstrated that there is a shortening of the cell cycle and a recruitment of growth-arrested cells to an active cycling state in psoriatic epidermis. It has been hypothesized that the increased epidermal thickness and altered tissue architecture . characteristic of psoriasis may be related to an abnormality in the apoptotic or programmed cell death pathway.

Apoptosis is a programmed cell death activated when cell removal is needed and the pathogenesis of cutaneous diseases may involve an imbalance in the homeostatic mechanisms determining whether the death of keratinocytes will occur by terminal differentiation or apoptosis. It has been hypothesized that the increased epidermal thickness and altered tissue architecture characteristic of psoriasis may be related to an abnormality in the apoptotic or programmed cell death pathway.

Commitment to death (apoptosis) in susceptible cells can be modified . by a set of proteins that can• re-affirm• or forestall the death sentence, and among these proteins Bch and p53 appear to have a major responsibility.

The most fully described and perhaps the most important set of death regulating proteins is the Bcl2 family.