Title of article :
Detection of Serotonin Transporter Protein and Bax Gene Expression in Psoriasis: A Possible Role in Regulating Apoptosis
Author/Authors :
Leheta, Tahra M. Cairo University - Faculty of Medicine - Department of Dermatology, Egypt , Rashed, Laila A. Cairo University - Faculty of Medicine - Department of Clinical Biochemistry, Egypt
From page :
28
To page :
33
Abstract :
Background. Psoriasis may occur or worsen in connection with stress or mood disorders. Serotonin (5-hydroxytryptamin; 5-HT), through its serotonin tran sporter (SERT) protein, may play a role in connection with different types of inflammation of the skin, including psoriasis. Keratinocyte apoptosis plays a fundamental part in the control of epidermal morphogenesis. Bax is a major regulator of apoptosis. Objective. To characterize the PCR expression of SERT protein as well as Bax gene in the involved psoriatic skin and to look for a possible correlation of SERT with Bax, which is a major regulator of apoptosis. Patients and methods. This prospective study included 20 patients with psoriasis and 20 healthy subjects free from inflammatory dermatoses to serve as a control group. Biopsies were taken from both patients and controls for PCR detection of SERT protein and Bax gene expression. Results. Statistical analysis revealed that the mean value of both the SERT and Bax in psoriatic patients was statistically significantly higher (p 0.001) than in the controls. This study also revealed positive significant correlation between SERT and Bax in both the psoriatic patients and the control group (p = 0.002). Conclusion. The apoptotic process may possibly be influenced by modulators of SERT, which may be of clinical relevance in connection with the treatment of psoriatic patients with antidepressants
Keywords :
Serotonin , transporter protein , Bax , gene , apoptosis , psoriasis
Journal title :
Journal of the Egyptian Women s Dermatologic Society
Journal title :
Journal of the Egyptian Women s Dermatologic Society
Record number :
2714870
Link To Document :
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