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노병화,김대현,조문균,박영립,황규왕 대한피부과학회 2008 Annals of Dermatology Vol.20 No.4
Background: Human skin is exposed to various environmental stresses, such as heat, cold, and ultraviolet (UV) radiation. Heat shock proteins (HSPs) induced by temperature elevations, as a physiologic response to mediate repair mechanisms and reduce cellular damage. Objective: The purpose of this study was to investigate the induction of HSPs in human skin cells after UV exposure. Methods: We performed immunoblotting using a specific monoclonal antibody to the HSP70 family, one of the best-conserved stress proteins in humans, with cultured normal human keratinocytes, A431 cells, human melanocytes, SK30 cells, and human dermal fibroblasts (HDF). Results: Our results indicated that high expression of HSP70 in the unstressed state was noted in epidermal cells, including normal human keratinocytes, A431 cells, human melanocytes, and SK30 cells, but epidermal cells showed no additional up-regulation of HSP70 after UV irradiation. On the other hand, HDF expressed very small amounts of HSP70 at baseline, but significantly higher amounts of HSP70 after UV exposure. Conclusion: These findings suggest that constitutive expression of HSP70 in epidermal cells may be an important mechanism for protection of the human epidermis from environmental stresses, such as sunlight exposure. Background: Human skin is exposed to various environmental stresses, such as heat, cold, and ultraviolet (UV) radiation. Heat shock proteins (HSPs) induced by temperature elevations, as a physiologic response to mediate repair mechanisms and reduce cellular damage. Objective: The purpose of this study was to investigate the induction of HSPs in human skin cells after UV exposure. Methods: We performed immunoblotting using a specific monoclonal antibody to the HSP70 family, one of the best-conserved stress proteins in humans, with cultured normal human keratinocytes, A431 cells, human melanocytes, SK30 cells, and human dermal fibroblasts (HDF). Results: Our results indicated that high expression of HSP70 in the unstressed state was noted in epidermal cells, including normal human keratinocytes, A431 cells, human melanocytes, and SK30 cells, but epidermal cells showed no additional up-regulation of HSP70 after UV irradiation. On the other hand, HDF expressed very small amounts of HSP70 at baseline, but significantly higher amounts of HSP70 after UV exposure. Conclusion: These findings suggest that constitutive expression of HSP70 in epidermal cells may be an important mechanism for protection of the human epidermis from environmental stresses, such as sunlight exposure.
노병화 ( Byoung Hwa Roh ),황규왕 ( Kyu Uang Whang ),조문균 ( Moon Kyun Cho ),박영립 ( Young Lip Park ),이종석 ( Jong Suk Lee ),이창우 ( Chang Woo Lee ) 대한피부과학회 2007 대한피부과학회지 Vol.45 No.7
Background: Pemphigus vulgaris is an autoimmune bullous dermatoses of skin and mucosa characterized by loss of adhesion between keratinocytes, a process known as acantholysis. Apoptosis, programmed cell death, may participate in pathogenesis of intercellular detachment and loss of cell-matrix interaction. Objective: This study was designed to investigate the induction of apoptosis in the pemphigus lesional epidermis and to elucidate the mechanism of apoptosis induced by pemphigus sera. Methods: Hoechst 33342 staining was performed to determine the induction of apoptosis in the pemphigus lesional epidermis. In addition, we used HaCaT cells treated with pemphigus sera and analyzed the expression of caspase-3, caspase-8, caspase-9 and bcl-2, bcl-xL, bax, bak by the RT-PCR method. Results: In Hoechst 33342 staining, typical findings of apoptosis were observed in the pemphigus lesional epidermis showing acantholysis. RT-PCR showed the upregulation of caspase group (caspase-3, caspase-8, caspase-9), the downregulation of antiapoptotic bcl-2 family (bcl-2, bcl-xL) and the upregulation of proapoptotic bcl-2 family (bax, bak). Conclusion: These results suggest that apoptosis may be associated with acantholysis of pemphigus lesional epidermis and may play an important role in the pathogenesis of pemphigus. (Korean J Dermatol 2007;45(7):650∼658)