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Biomedical subjects

Kyoung Chan Park

Publications and source records attributed to Kyoung Chan Park.

6 recordsLinked to original sources

The effect of substance P on peripheral blood mononuclear cells in patients with atopic dermatitis.

BACKGROUND: There is increasing evidence that neuropeptides, especially substance P (SP), may be involved in the pathogenesis of atopic dermatitis (AD). OBJECTIVE: We performed this study to determine more precisely the role of SP in AD. METHODS: We separated peripheral blood mononuclear cells (PBMCs) from AD patients and normal controls, and measured proliferation response and cytokine release after adding SP (10(-11), 10(-10) and 10(-9) M). We also compared substance P receptor expression by semi-quantitative RT-PCR. RESULTS: PBMCs from AD patients proliferated at significantly higher rates (ca. by 30%). Semi-quantitative RT-PCR showed that the level of expression of SP receptor increased in AD patients versus normal controls. IL-4 release from PBMCs was significantly higher in AD patients, while IFN-gamma release from PBMCs was significantly lower in AD patients. Different concentrations of SP did not cause any difference in IL-4 and IFN-gamma secretions. However, TNF-alpha release from PBMCs in AD patients increased significantly at 10(-10) and 10(-9) M of SP compared to SP (-) control. IL-10 release from PBMCs increased significantly in AD patients with 10(-9) M of SP compared to SP (-) control. CONCLUSION: SP might aggravate AD by increasing the production of TNF-alpha and IL-10 rather than by affecting IL-4 and IFN-gamma. This different immune response is considered to be the result of upregulated SP receptor in AD.

Adult↗

Impaired repair ability of hsp70.1 KO mouse after UVB irradiation.

UV light is absorbed in the epidermis and induces sunburn cell formation. It has been reported that HSP70 increases the UVB resistance of cell lines by in vitro experiments using various cell lines. In this study, hsp70.1(-/-) KO mouse was used in order to study the role of HSP70 after UVB irradiation. Western blotting showed a decreased level of HSP70 in hsp70.1(-/-) KO mouse compared with wild type FVB mouse. Six h after UVB irradiation, there were no significant histologic differences between the hsp70.1(-/-) KO mouse and the wild type FVB mouse. A similar degree of nuclear swelling was observed. However, there were significant differences at 12 and 24 h after UVB irradiation. After 12 h, a few apoptotic cells were observed in the wild type mouse, but a large number of cells were apoptotic in the hsp70.1(-/-) KO mouse. After 24 h, the epidermis of the wild type FVB mouse was relatively intact, but almost the entire epidermis was necrotic in the hsp70.1(-/-) KO mouse. These results showed that epidermal injury of hsp70.1(-/-) KO mouse was much more severe than that of wild type mouse although initial changes are similar in both species of mice. These results suggest that susceptibility of hsp70.1(-/-) KO mouse to UVB irradiation may originate from a defect in the repair mechanism. This HSP deficient model may be useful in studies of the effects of tissue injury that relate to the impaired tissue repair mechanisms.

Animals↗

Effects of C2-ceramide on the Malme-3M melanoma cell line.

Ceramide is implicated in the regulation of various signaling pathways leading to proliferation, differentiation or apoptotic cell death, but there have been few investigations about the effects of ceramide on the cell growth and the melanogenesis of melanocytes. In the present study, we investigated the effects of cell-permeable ceramide on Malme-3M human melanoma cell line. MTT proliferation assay showed that C2-ceramide inhibited the growth of Malme-3M cells in a dose-dependent manner. Cell cycle analysis confirmed the inhibition of DNA synthesis by a reduction in the S phase and an increase in the G0/G1 phase. Flow cytometric analysis for apoptotic cells and morphological observations indicated that the antiproliferative effect of C2-ceramide was not due to apoptosis. We next investigated the effects of C2-ceramide on the pigmentation of Malme-3M melanoma cells. The results showed that C2-ceramide induced only a slight decrease of tyrosinase activity and melanin synthesis. To investigate the ceramide signaling pathway, we studied the influence of C2-ceramide on extracellular signal-regulated kinase (ERK) and Akt activation by Western blot. We demonstrated that the amount of phosphorylated Akt was decreased by C2-ceramide, whereas ERK was activated transiently. Because of a well-known involvement of ceramide in apoptosis, we further investigated the level of caspase-3 and HSP70 after treatment of C2-ceramide. We found that the caspase-3 was not activated and the expression of HSP70 increased moderately. In conclusion, C2-ceramide inhibited the cell growth of Malme-3M cells without the induction of apoptosis. We suggest that increased HSP70 may be related to the resistance against apoptosis.

Cell Cycle↗

Fibroblasts and ascorbate regulate epidermalization in reconstructed human epidermis.

Skin equivalent model provides a new investigating system to study the role of extracellular matrix and dermal factors such as collagen, basement membrane components and fibroblasts (Fb) which contribute to cell-cell and cell-matrix interactions. Although basement membrane factors is known to play an important role in epidermal differentiation and epidermal-matrix adhesion, comparative effects of these extracellular matrix and dermal factors on the reconstruction of epidermis are little known. In this study, we investigated effects of type I collagen (Coll I), type IV collagen plus laminin (LAM) coated Coll I (Coll IV+LAM), and human Fb enriched Coll I (Coll I+Fb) on epidermal reconstruction. When human keratinocytes were cultured on three different gels containing Coll I, Coll IV+LAM and Coll I+Fb, basal keratinocytes were cuboidal and perpendicular to the dermo-epidermal junction only in the gel containing Coll I+Fb. Proliferation marker expression was prominent and differentiation marker expression was similar with those of normal skin in the gel containing Coll I+Fb than in the other gel models. Since ascorbate is suspected to exert an effect as a modulator of proliferation and differentiation in keratinocytes, we tested the effects of ascorbate on human epidermis reconstruction. When 25 microg/ml ascorbate was added, disordered arrangement of epidermis was disappeared and differentiation marker expression was similar with its expression in normal skin. These data indicate that human Fb and a modulator of proliferation and differentiation such as ascorbate are essential for epidermalization in reconstructed epidermis.

Ascorbic Acid↗

Evaluation of facial skin type by sebum secretion: discrepancies between subjective descriptions and sebum secretion.

BACKGROUND/AIMS: Facial skin is usually classified as dry, normal, and oily in the cosmetics field. However, there is no standard objective method for classifying facial skin. METHODS: We measured sebum excretion with Sebumeter at four sites on the face. Based on the amount of sebum secretion, we reclassified skin type according to the guidelines provided by the manufacturer. The mean of sebum excretion (mean facial sebum excretion; MFSE) was also calculated. RESULTS: People secrete varying amounts of sebum at different skin sites. Reclassification of skin type based on sebum secretion revealed that most participants underestimated the amount of facial sebum excretion. When sebum secretion amounts were compared, a statistically significant difference was apparent between the oily and dry skin types. However, there were no statistical differences between oily and normal, and normal and dry skin. CONCLUSION: We showed that subjective skin type does not match the amount of sebum secreted. Thus, this simple and subjective classification is of very limited use and it should be re-evaluated by using an objective and standardized measuring tool.

Adult↗

Fructose-1,6-diphosphate attenuates prostaglandin E2 production and cyclo-oxygenase-2 expression in UVB-irradiated HaCaT keratinocytes.

1. Fructose-1,6-diphosphate (FDP), a glycolytic metabolite, is reported to ameliorate inflammation and inhibit the nitric oxide production in murine macrophages stimulated with endotoxin. It is also reported that FDP has cytoprotective effects against hypoxia or ischaemia/reperfusion injury in brain and heart. However, underlying mechanisms of its various biological activities are not completely understood. 2. In this study, we examined the effects of FDP on UVB-induced prostaglandin production in HaCaT keratinocytes. 3. Ultraviolet B (UVB, 280-320 nm) irradiation (30 mJ cm(-2)) increased prostaglandin E(2)(PGE(2)) production, which was significantly decreased by FDP in a concentration dependent manner. NS-398, a cyclo-oxygenase-2 (COX-2) selective inhibitor completely inhibited UVB-induced PGE(2) production showing that COX-2 activity is responsible for the increase in PGE(2) production under our experimental conditions. 4. UVB irradiation increased total COX activity and COX-2 mRNA in HaCaT keratinocytes, which were significantly blocked by FDP in a concentration dependent manner. 5. N-acetylcysteine (NAC) significantly attenuated UVB-induced PGE(2) production, COX activity and COX-2 mRNA expression indicating oxidative components might contribute to these events. 6. FDP reduced UVB-induced increase in cellular reactive oxygen species (ROS) level although it did not show direct radical scavenging effect in the experiment using 1,1-diphenyl-2picrylhydrazil (DPPH). FDP preserved the cellular antioxidant capacity including catalase activity and GSH content after irradiation. 7. Our data obtained hitherto suggest that FDP may have a protective role in UVB-injured keratinocyte by attenuating PGE(2) production and COX-2 expression, which are possibly through blocking intracellular ROS accumulation.

Cell Line↗