KMID : 0604220050120040113
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Korean Journal Investigative Dermatology 2005 Volume.12 No. 4 p.113 ~ p.122
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Park Soo-Ji
Park Young-Lip Lee Jong-Suk Cho Moon-Kyun Whang Kyu-Uang
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Abstract
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Psoriasis is a chronic hyperproliferative inflammatory skin disease. The pathogenesis of psoriasis is considered increase of epidermal keratinocyte survival caused by increase of epidermal mitosis and inhibition of epidermal apoptosis. Keratinocyte apoptosis plays a fundamental part in the control of epidermal morphogenesis and homeostasis. Proliferation of keratinocytes is restricted by apoptotic cell death to maintain a constant thickness of epidermis.
The regulation of this process involves a dynamic interaction between death-accelerator and death- depressor proteins. Several proteins of the bcl gene family are involved in the regulation programmed cell death either by preventing(bcl-2, bcl-xL) or by promoting apoptosis(bax, bak, bad). The caspase group is a protease which is essential for the apoptosis. Apoptosis is processed by initiator caspase(caspase-8, caspase-9) and effector caspase(caspase-3). Psoriasis is considered apoptotic mechanism is inhibited and that is affected by bcl-2 protein family balance and caspase group expression.
We investigated the expression of bcl-2 protein family(bcl-2, bcl-xL, bax, bak, bad) and caspase group (caspase-3, 8, 9) in cultured keratinocyte in psoriasis serum using RT-PCR for the purpose of studying the association of psoriasis and apoptosis.
RT-PCR showed increased expression of bcl-xL, and decreased expression of bcl-2, bax, bak, bad in bcl-2 protein family. And RT-PCR showed decreased all of the expression of caspase-3, 7, 9.
It suggested that apoptotic mechanism is inhibited generally in Psorisis by increase of antiapoptotic bcl-2 family expression(bcl-xL) and decrease of proapoptotic bcl-2 family expression(bax, bak, bad). Furthermore, it is supported by the decreased activity of caspase group(caspase-3, 8, 9).
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KEYWORD
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Psoriasis, Apoptosis, bcl-2 protein family, Caspase
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