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- 발행기관 : The Society for Investigative Dermatology, Inc (검색결과 60 건)
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EC-SOD Suppresses Contact Hypersensitivity in Mouse Skin by Impairing Langerhans Cell Migration
Na, Kwangmin,Kim, Kyoung-Eun,Park, Sang-Tae,Kim, Tae-Yoon The Society for Investigative Dermatology, Inc 2007 The Journal of investigative dermatology Vol.127 No.8
Extracellular superoxide dismutase (EC-SOD) is primarily a tissue enzyme and has been implicated in the modulation of inflammatory response. The biological role of EC-SOD in skin, however, has rarely been investigated. In this study, we aim to explore the effects of EC-SOD on the inflammatory response in skin by evaluating the contact hypersensitivity response (CHS) in EC-SOD transgenic mice. Transgenic mice with skin-specific expression of EC-SOD were sensitized and challenged with 2,4,6-trinitro-1-chlorobenzene (TNCB), followed by measurement of ear swelling. EC-SOD transgenic mice showed significantly reduced CHS responses compared with wild-type mice. Histological evaluation of the challenged ears of EC-SOD transgenic mice revealed diminished infiltration of inflammatory cells with a failure to induce expression of inflammatory cytokines, such as tumor necrosis factor-α and IFN-γ, on sensitization and challenge with TNCB. Furthermore, Langerhans cell migration to lymph nodes was impaired in EC-SOD transgenic mice. These results indicate that EC-SOD downregulates CHS through inhibition of the inflammatory response, suggesting a possible therapeutic regimen in inflammatory skin diseases.Journal of Investigative Dermatology (2007) 127, 1930–1937; doi:10.1038/sj.jid.5700802; published online 29 March 2007
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Lee, Eun-Jung,Lee, Yun Sang,Hwang, Soonho,Kim, Sanghee,Hwang, Jae Sung,Kim, Tae-Yoon The Society for Investigative Dermatology, Inc 2011 The Journal of investigative dermatology Vol.131 No.8
Melanin protects the skin from harmful environmental factors such as UV light. However, excessive melanin production induces hyperpigmentation. Previously, N-(3,5-dimethylphenyl)-3-methoxybenzamide (A<SUB>3</SUB>B<SUB>5</SUB>), a biaryl amide derivative, was identified for its ability to inhibit melanin production. However, its detailed mechanism of action has not been investigated. We elucidated the inhibitory mechanisms of A<SUB>3</SUB>B<SUB>5</SUB> in melanin production. Our results showed that A<SUB>3</SUB>B<SUB>5</SUB> had no effect on the production and activity of tyrosinase, an enzyme involved in melanogenesis. However, A<SUB>3</SUB>B<SUB>5</SUB> markedly decreased both constitutively expressed and UVB-induced tyrosinase-related protein 2 (TRP-2), which plays an important role along with tyrosinase in melanogenesis. The TRP-2 downregulation caused by A<SUB>3</SUB>B<SUB>5</SUB> may occur through proteasomal degradation because the A<SUB>3</SUB>B<SUB>5</SUB>-induced TRP-2 downregulation was inhibited by the ubiquitination inhibitor, MG-132. In addition, A<SUB>3</SUB>B<SUB>5</SUB> inhibited the proliferation of melanocytes and melanoma cells by arresting cells in the G1 stage of the cell cycle and moderately suppressed tumor growth in vivo. Taken together, our results indicate that A<SUB>3</SUB>B<SUB>5</SUB> downregulates melanin production and melanoma cell growth via proteosomal degradation of TRP-2 and suggest that A<SUB>3</SUB>B<SUB>5</SUB> can be a possible therapeutic agent that effectively regulates both hyperpigmentation and melanoma growth in the skin.
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Park, Gyuman,Yoon, Byung Sun,Moon, Jai-Hee,Kim, Bona,Jun, Eun Kyoung,Oh, Sejong,Kim, Hyunggee,Song, Hea Joon,Noh, Joo Young,Oh, ChilHwan,You, Seungkwon The Society for Investigative Dermatology, Inc 2008 The Journal of investigative dermatology Vol.128 No.10
Keloids are benign skin tumors characterized by collagen accumulation and hyperproliferation of fibroblasts. To find an effective therapy for keloids, we explored the pharmacological potential of (−)-epigallocatechin-3-gallate (EGCG), a widely investigated tumor-preventive agent. When applied to normal and keloid fibroblasts (KFs) in vitro, proliferation and migration of KFs were more strongly suppressed by EGCG than normal fibroblast proliferation and migration (IC<SUB>50</SUB>: 54.4 μM (keloid fibroblast (KF)) versus 63.0 μM (NF)). The level of Smad2/3, signal transducer and activator of transcription-3 (STAT3), and p38 phosphorylation is more enhanced in KFs, and EGCG inhibited phosphorylation of phosphatidylinositol-3-kinase (PI3K), extracellular signal-regulated protein kinase 1/2 (ERK1/2), and STAT3 (Tyr705 and Ser727). To evaluate the contribution of these pathways to keloid pathology, we treated KFs with specific inhibitors for PI3K, ERK1/2, or STAT3. Although a PI3K inhibitor significantly suppressed proliferation, PI3K and MEK/ERK inhibitors had a minor effect on migration and collagen production. However, a JAK2/STAT3 inhibitor and a STAT3 siRNA strongly suppressed proliferation, migration, and collagen production by KFs. We also found that treatment with EGCG suppressed growth and collagen production in the in vivo keloid model. This study demonstrates that EGCG suppresses the pathological characteristics of keloids through inhibition of the STAT3-signaling pathway. We propose that EGCG has potential in the treatment and prevention of keloids.Journal of Investigative Dermatology (2008) 128, 2429–2441; doi:10.1038/jid.2008.103; published online 8 May 2008
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Collagen Synthesis Is Suppressed in Dermal Fibroblasts by the Human Antimicrobial Peptide LL-37
Park, Hyun Jeong,Cho, Dae Ho,Kim, Hee Jung,Lee, Jun Young,Cho, Baik Kee,Bang, Sa Ik,Song, Sang Yong,Yamasaki, Kenshi,Di Nardo, Anna,Gallo, Richard L The Society for Investigative Dermatology, Inc 2009 The Journal of investigative dermatology Vol.129 No.4
LL-37 is a human cathelicidin antimicrobial peptide that is released in the skin after injury and acts to defend against infection and modulate the local cellular immune response. We observed in human dermal keloids that fibrosis was inversely related to the expression of cathelicidin and sought to determine how LL-37 influenced expression of types I and III collagen genes in dermal fibroblasts. At nano-molar concentrations, LL-37 inhibited baseline and transforming growth factor-β-induced collagen expression. At these concentrations, LL-37 also induced phosphorylation of extracellular signal-regulated kinase (ERK) within 30 minutes. Activation of ERK, and the activation of a G-protein-dependent pathway, was essential for inhibition of collagen expression as pertussis toxin or an inhibitor of ERK blocked the inhibitory effects of LL-37. c-Jun N-terminal kinase and p38 mitogen-activated protein kinase inhibitors did not alter the effects of cathelicidin. Silencing of the Ets-1 reversed inhibitory effects of LL-37. Taken together, these findings show that LL-37 can directly act on dermal fibroblasts and may have antifibrotic action during the wound repair process.Journal of Investigative Dermatology (2009) 129, 843–850; doi:10.1038/jid.2008.320; published online 16 October 2008
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Li, Wen H,Lee, Young M,Kim, Jee Y,Kang, Seokwon,Kim, Sangmin,Kim, Kyu H,Park, Chi-Hyun,Chung, Jin H The Society for Investigative Dermatology, Inc 2007 The Journal of investigative dermatology Vol.127 No.10
Transient receptor potential vanilloid-1 (TRPV1), a heat-gated channel, was recently found on human keratinocytes and the activation of epidermal TRPV1 was known to induce release of proinflammatory mediators. However, the functional consequences of TRPV1 activation in cutaneous physiology and pathology have not been elucidated clearly. In this study, we investigated the role of TRPV1 on the matrix metalloproteinase (MMP)-1 expression induced by heat shock in human epidermal keratinocytes. Heat shock induced the expression of MMP-1 mRNA and protein in a temperature-dependent manner in an immortalized human keratinocyte cell line (HaCaT) and normal human epidermal keratinocytes (NHK). Heat-shock-induced MMP-1 expression was decreased by treatment of the TRPV1 inhibitors (capsazepine and ruthenium red) or knockdown of TRPV1 using RNA interference in HaCaT cells. Overexpression of TRPV1 greatly increased heat-shock-induced MMP-1 promoter activity in HEK 293 cells. Furthermore, direct activation of TRPV1 by capsaicin, a TRPV1 agonist, increased MMP-1 expression. We found that heat shock induced calcium influx through TRPV1 and that extracellular calcium was necessary for heat-shock-induced MMP-1 expression in HaCaT cells. Taken together, our results suggest that heat-shock-induced MMP-1 expression is mediated by activation of TRPV1 and is dependent on a calcium-dependent signaling process in human epidermal keratinocytes.Journal of Investigative Dermatology (2007) 127, 2328–2335; doi:10.1038/sj.jid.5700880; published online 17 May 2007
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Lee, Woong-Hee,Jang, Sunhyae,Lee, Jung-Suk,Lee, Young,Seo, Eun-Young,You, Kwan-Hee,Lee, Seung-Chul,Nam, Kwang-Il,Kim, Jin-Man,Kee, Sun-Ho,Yang, Jun-Mo,Seo, Young- Joon,Park, Jang-Kyu,Kim, Chang Deok,L The Society for Investigative Dermatology, Inc 2005 The Journal of investigative dermatology Vol.125 No.5
We isolated a human gene encoding keratinocyte proline-rich protein (hKPRP). hKPRP gene is located in the region of epidermal differentiation complex on chromosome 1q21, and its ∼2.5 kb mRNA encodes 579 amino acid protein with high proline content (18%). The mRNA level of hKPRP was markedly increased at both 7 and 14 d after treatment with 1.2 mM calcium in cultured normal human epidermal keratinocytes. In situ hybridization demonstrated that hKPRP was expressed in upper granular layer of normal epidermis with characteristic intermittent pattern. In psoriatic lesion, hKPRP expression was increased as compared with normal skin and showed continuous pattern. Immunohistochemical analysis also confirmed the expression of hKPRP at the protein level. Western blot analysis showed that hKPRP protein of ∼70 kDa size was significantly increased by calcium in a time-dependent manner. In mouse tissue blot assays, the expression of KPRP was detected in stomach and skin tissues, and began at 17.5 embryonic days. Additionally, hKPRP expression was detected in the periderm of human fetal skin from 16 wk estimated gestational age. Together, these results suggest that hKPRP is an epidermal marker expressed in stratified squamous epithelia and has a potential role in keratinocytes differentiation.Journal of Investigative Dermatology (2005) 125, 995–1000; doi:10.1111/j.0022-202X.2005.23887.x
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LXRα Enhances Lipid Synthesis in SZ95 Sebocytes
Hong, Il,Lee, Min-Ho,Na, Tae-Young,Zouboulis, Christos C,Lee, Mi-Ock The Society for Investigative Dermatology, Inc 2008 The Journal of investigative dermatology Vol.128 No.5
Differentiation of sebocytes is strongly associated with enhanced lipid synthesis and accumulation in the cells. Liver X receptors (LXRs) are members of the nuclear receptor superfamily, which play a critical role in cholesterol homeostasis and lipid metabolism. We examined whether LXRα regulated lipid synthesis in the immortalized human sebaceous gland cell line SZ95. When the SZ95 sebocytes were treated with the ligand of LXR such as TO901317 or 22(R)-hydroxycholesterol, lipid droplets were accumulated in the majority of cells when examined by Oil Red O staining. The expression of the known LXR targets, such as fatty acid synthase and sterol regulatory-binding protein-1, was induced by TO901317. TO901317 treatment increased expression of LXRα but not that of LXRβ. Transfection of antisense LXRα significantly decreased TO901317-induced target gene expression and lipid droplet accumulation, suggesting a major role of LXRα in differentiation of sebocytes. Further, TO901317 decreased the expression of cyclooxygenase-2 and inducible nitric oxide synthase that was induced by lipopolysaccharide treatment. Together, these results indicate that important roles of LXRα in differentiation and inflammatory signaling in sebaceous glands. Thus, we suggest that LXR ligands could provide a new class of therapeutic agents for sebaceous gland-associated disorders such as seborrhea and acne.Journal of Investigative Dermatology (2008) 128, 1266–1272; doi:10.1038/sj.jid.5701134; published online 25 October 2007
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Suppression of Spontaneous Dermatitis in NC/Nga Murine Model by PG102 Isolated from Actinidia arguta
Park, Eun-Jin,Park, Kyoung Chul,Eo, Haekwan,Seo, Jangkyun,Son, Miwon,Kim, Kyu Han,Chang, Yoon-Seok,Cho, Sang-Heon,Min, Kyung-Up,Jin, Mirim,Kim, Sunyoung The Society for Investigative Dermatology, Inc 2007 The Journal of investigative dermatology Vol.127 No.5
Atopic dermatitis (AD) is a chronic inflammatory skin disease, which requires safe and effective pharmacological therapy. We previously found that two preparations from Actinidia arguta, PG102T, and PG102E, could modulate Th1/Th2 pathways and suppress IgE biosynthesis. This study was performed to assess the therapeutic effects of PG102T and PG102E on the development of dermatitis in NC/Nga mice, characterized by the spontaneous onset of AD along with an elevated level of IgE under conventional conditions. PG102T or PG102E administration significantly reduced dermatitis severity as well as scratching tendency in conventional mice. The suppression of dermatitis by PG102 was accompanied by a decrease in the plasma level of IgE, IgG1, and IL-4 and also by an increase in that of IgG2a and IL-12. The splenic level of IL-4, IL-5, and IL-10 was downregulated, whereas that of IFN-γ and IL-12 was increased. The number of eosinophils and the expression of eotaxin and thymus and activation-regulated chemokine were decreased by PG102T or PG102E. Histological findings also indicated that the thickening of epidermis/dermis and the dermal infiltration of inflammatory cells including mast cells were greatly inhibited. These data suggest that PG102 may be effective therapeutic agents for the treatment of AD.Journal of Investigative Dermatology (2007) 127, 1154–1160. doi:10.1038/sj.jid.5700658; published online 28 December 2006
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Lee, Youngae,Kim, Hyunjung,Kim, Sangmin,Shin, Mi Hee,Kim, Yeon Kyung,Kim, Kyu Han,Chung, Jin Ho The Society for Investigative Dermatology, Inc 2009 The Journal of investigative dermatology Vol.129 No.2
Myeloid differentiation factor 88 (MyD88) is known as an adaptor protein for the Toll-like receptor (TLR) family and participates in signal transduction by binding to the cytoplasmic Toll/IL-1 receptor (TIR) domains of activated TLR. In this study, we demonstrated that expression of MyD88 is increased in photoaged skin compared with intrinsic aged human skin of the same elderly individuals, and that acute UV irradiation increases MyD88 expression in human skin in vivo. To investigate the effects of these high levels of MyD88 in photoaged skin and acutely UV-irradiated skin, human epidermal keratinocytes were infected with adenovirus expressing wild-type (MyD88wt), dominant-positive (MyD88ΔC), and dominant-negative (MyD88ΔN) MyD88 forms. Overexpression of MyD88wt and MyD88ΔC, but not of MyD88ΔN, increased the basal expressions of IL-6 and matrix metalloproteinase-1 (MMP-1) in human epidermal keratinocytes. Moreover, overexpression of MyD88ΔN prevented UV-induced expressions of IL-6 and MMP-1 by inhibiting UV-induced activation of NF-κB and activating protein-1. These results suggest that MyD88 is important in IL-6 and MMP-1 expressions in both acutely UV-irradiated skin and in chronically sun-exposed human skin.Journal of Investigative Dermatology (2009) 129, 460–467; doi:10.1038/jid.2008.261; published online 21 August 2008
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