Journal of Dermatological Science Supplement最新文献_第2页

Cytokine profiles of skin lesions in murine lupus models 小鼠狼疮模型皮肤损伤的细胞因子谱

Journal of Dermatological Science Supplement Pub Date : 2005-12-01 DOI: 10.1016/J.DESCS.2005.06.005

T. Nishide, T. Yoshimasu, T. Ikeda, N. Seo, T. Ohtani, F. Furukawa

引用次数: 9

Ultraviolet (UV) light irradiation induced signal transduction in skin photoaging 紫外线照射诱导皮肤光老化的信号转导

Journal of Dermatological Science Supplement Pub Date : 2005-12-01 DOI: 10.1016/j.descs.2005.06.002

Yiru Xu, Gary J. Fisher

{"title":"Ultraviolet (UV) light irradiation induced signal transduction in skin photoaging","authors":"Yiru Xu, Gary J. Fisher","doi":"10.1016/j.descs.2005.06.002","DOIUrl":"https://doi.org/10.1016/j.descs.2005.06.002","url":null,"abstract":"<div><p><span><span>The purpose of this article is to offer perspective on current understanding of ultraviolet (UV) irradiation-induced signal transduction, with emphasis on membrane-initiated, non-nuclear signaling events. We will describe the role of UV-induced signaling in the mechanism of premature skin aging (photoaging). UV irradiation serves as a universal ligand to active </span>cell surface receptors<span><span> and to induce assembly of signaling complexes at the plasma membrane. These complexes activate cytosolic protein kinase cascades that relay signals to the </span>cell nucleus, thereby regulating the activity of a variety transcription factors. Key cellular responses are up-regulation of matrix-degrading </span></span>metalloproteinases<span>, and down-regulation of extracellular matrix biosynthesis. The resultant net deficit of structural integrity of skin connective tissue is one of the major factors that contributes to the phenotype of photoaging. Insights into the molecular mechanisms of UV-induced signal transduction will eventually translate into new, effective methods to prevent UV-induced skin damage.</span></p></div>","PeriodicalId":100772,"journal":{"name":"Journal of Dermatological Science Supplement","volume":"1 2","pages":"Pages S1-S8"},"PeriodicalIF":0.0,"publicationDate":"2005-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.descs.2005.06.002","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91721356","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 103

Cytokine profiles of skin lesions in murine lupus models 小鼠狼疮模型皮肤损伤的细胞因子谱

Journal of Dermatological Science Supplement Pub Date : 2005-12-01 DOI: 10.1016/j.descs.2005.06.005

Takeshi Nishide , Takashi Yoshimasu , Takaharu Ikeda , Naohiro Seo , Toshio Ohtani , Fukumi Furukawa

{"title":"Cytokine profiles of skin lesions in murine lupus models","authors":"Takeshi Nishide , Takashi Yoshimasu , Takaharu Ikeda , Naohiro Seo , Toshio Ohtani , Fukumi Furukawa","doi":"10.1016/j.descs.2005.06.005","DOIUrl":"https://doi.org/10.1016/j.descs.2005.06.005","url":null,"abstract":"<div><h3>Background</h3><p>Skin lesions of cutaneous lupus erythematosus (LE) have a number of infiltrating T cells, and these T cells and their related cytokines are involved in the development of skin lesions.</p></div><div><h3>Objective</h3><p>In order to verify the roles of T cells and their related cytokines, we compared the cytokine profiles of LE-like skin lesions in experimentally-induced knock out (KO) mice and autoimmune-prone mice.</p></div><div><h3>Methods</h3><p>Lesional skin samples were obtained from CD4 KO mice and TCRα KO mice of the B6 background treated with ultraviolet B light (UVBL) and fluorouracil (FU), and MRL/lpr mice. The levels of mRNAs for TNF-α, IFN-γ, IL-2, IL-4, IL-10 and IL-12 were determined by RT-PCR in these skin samples.</p></div><div><h3>Results</h3><p>Combination treatment with UVBL and FU to TCRα KO mice and CD4 KO mice revealed the importance of CD4<sup>+</sup> CD8<sup>−</sup> γδT cells in the induction of drug induced cutaneous LE. Moreover, IL-12, IFN-γ and TNF-α were upregulated in TCRα KO mice treated with UVBL and FU. In contrast, IFN-γ was not elevated in the spontaneous LE-like skin lesions of MRL/lpr mice.</p></div><div><h3>Conclusions</h3><p>Cytokine profile pattern varies from strain to strain, and that murine cutaneous LE models, like human LE patients, manifest a wide range of immunological abnormalities, including cytokines.</p></div>","PeriodicalId":100772,"journal":{"name":"Journal of Dermatological Science Supplement","volume":"1 2","pages":"Pages S37-S43"},"PeriodicalIF":0.0,"publicationDate":"2005-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.descs.2005.06.005","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91721354","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 9

A novel anti-photoaging ingredient with the effect of iron sequestering 一种具有固铁作用的新型抗光老化成分

Journal of Dermatological Science Supplement Pub Date : 2005-12-01 DOI: 10.1016/J.DESCS.2005.06.006

Y. Ishitsuka, Misako Kobayashi, K. Arakane, Tadashi Suzuki, M. Kitazawa, T. Nakano, K. Iwasaki, K. Sakamoto

引用次数: 2

Ultraviolet (UV) light irradiation induced signal transduction in skin photoaging 紫外线照射诱导皮肤光老化的信号转导

Journal of Dermatological Science Supplement Pub Date : 2005-12-01 DOI: 10.1016/J.DESCS.2005.06.002

Yiru Xu, G. Fisher

引用次数: 105

A novel anti-photoaging ingredient with the effect of iron sequestering 一种具有固铁作用的新型抗光老化成分

Journal of Dermatological Science Supplement Pub Date : 2005-12-01 DOI: 10.1016/j.descs.2005.06.006

Yukiko Ishitsuka , Misako Kobayashi , Kumi Arakane , Tadashi Suzuki , Manabu Kitazawa , Takashi Nakano , Keiji Iwasaki , Kazutami Sakamoto

{"title":"A novel anti-photoaging ingredient with the effect of iron sequestering","authors":"Yukiko Ishitsuka , Misako Kobayashi , Kumi Arakane , Tadashi Suzuki , Manabu Kitazawa , Takashi Nakano , Keiji Iwasaki , Kazutami Sakamoto","doi":"10.1016/j.descs.2005.06.006","DOIUrl":"https://doi.org/10.1016/j.descs.2005.06.006","url":null,"abstract":"<div><h3>Background</h3><p>The reactive oxygen species generated by ultraviolet rays causes various types of cutaneous damage, such as lipid peroxidation and denaturation of the extra-cellular matrix. The accumulation of such damage contributes to skin aging, especially the formation of wrinkles. It has been suggested that iron ions, released from iron-binding proteins by ultraviolet rays, promote the production of radicals and accelerate the formation of wrinkles. Thus, sequestering iron ions might be effective in suppressing wrinkle formation.</p></div><div><h3>Objective</h3><p>Our purpose is to develop new cosmetic materials with iron sequesteing capacity to suppress skin photoaging, especially wrinkle formation.</p></div><div><h3>Method</h3><p>We designed a novel compound, <em>N</em>-(4-pyridoxylmethylene)-<span>l</span>-serine (PYSer), as a cosmetic material with a structure similar to a biological iron sequestering protein. We studied its effect on suppressing hydroxyl radical generation and wrinkle formation in a mouse model for skin photoaging.</p></div><div><h3>Results</h3><p>PYSer almost completely inhibited the generation of hydroxyl radicals by iron ions. In contrast, EDTA<span>, a typical metal chelator, did not suppress hydroxyl radical production, but enhanced it. Furthermore, PYSer delayed UVB-induced wrinkle formation and skin thickening.</span></p></div><div><h3>Conclusion</h3><p>This study demonstrates that PYSer suppresses photoaging, particularly, wrinkle formation and skin thickening.</p></div>","PeriodicalId":100772,"journal":{"name":"Journal of Dermatological Science Supplement","volume":"1 2","pages":"Pages S45-S52"},"PeriodicalIF":0.0,"publicationDate":"2005-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.descs.2005.06.006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91721355","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

DNA repair initiated by glycosylases in the nucleus and mitochondria of mammalian cells; how our cells respond to a flood of oxidative DNA damage 哺乳动物细胞核和线粒体中糖基酶启动的DNA修复我们的细胞是如何应对大量氧化性DNA损伤的

Journal of Dermatological Science Supplement Pub Date : 2005-12-01 DOI: 10.1016/j.descs.2005.06.001

Masashi Takao, Akira Yasui

{"title":"DNA repair initiated by glycosylases in the nucleus and mitochondria of mammalian cells; how our cells respond to a flood of oxidative DNA damage","authors":"Masashi Takao, Akira Yasui","doi":"10.1016/j.descs.2005.06.001","DOIUrl":"https://doi.org/10.1016/j.descs.2005.06.001","url":null,"abstract":"<div><p><span><span>Oxidative DNA damage causes blocks in transcription and replication and introduces errors leading to cell death and </span>genomic instability<span>. Extensive molecular analysis of repair mechanisms for oxidative DNA damage has revealed the strategy of mammalian cells against the threat posed by reactive oxygen species to the genetic information. Most oxidative base damage is first recognized by various glycosylases, which remove the base and initiate </span></span>base excision repair<span>, a repair mechanism widely distributed in life. However, disruptions of glycosylase genes have shown either no effect or rather mild phenotypes in mice, suggesting that the frontline defence against oxidative DNA damage has back-up systems. Indeed, a number of novel DNA glycosylases<span><span> with overlapping substrate specificity were recently identified in mammalian cells. Several glycosylases are transported into the mitochondria too, indicating the importance of glycosylases and base damage repair in the </span>mitochondria genome. Thus, mammalian cells survive the flood of oxidative DNA damage by means of extensive repair of the damage. Besides repair of DNA damage, mechanisms for tolerating DNA damage at replication have recently been discovered. Cells may tolerate residual damage at replication but thereby risk generating mutations.</span></span></p></div>","PeriodicalId":100772,"journal":{"name":"Journal of Dermatological Science Supplement","volume":"1 2","pages":"Pages S9-S19"},"PeriodicalIF":0.0,"publicationDate":"2005-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.descs.2005.06.001","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91721357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 6

Decrease of antioxidants and the formation of oxidized diacylglycerol in mouse skin caused by UV irradiation 紫外线照射引起小鼠皮肤抗氧化剂的减少和氧化二酰基甘油的形成

Journal of Dermatological Science Supplement Pub Date : 2005-12-01 DOI: 10.1016/j.descs.2005.06.003

Yutaka Tanino , Arief Budiyanto , Masato Ueda , Akihiro Nakada , Wei Tak Nyou , Makoto Yanagisawa , Masamitsu Ichihashi , Yorihiro Yamamoto

引用次数: 8

DNA repair initiated by glycosylases in the nucleus and mitochondria of mammalian cells; how our cells respond to a flood of oxidative DNA damage 哺乳动物细胞核和线粒体中糖基酶启动的DNA修复我们的细胞是如何应对大量氧化性DNA损伤的

Journal of Dermatological Science Supplement Pub Date : 2005-12-01 DOI: 10.1016/J.DESCS.2005.06.001

M. Takao, A. Yasui

引用次数: 6

Sex ratio in the children of Yusho patients 玉树病人子女的性别比例

Journal of Dermatological Science Supplement Pub Date : 2005-04-01 DOI: 10.1016/j.descs.2005.03.014

T. Uenotsuchi, Y. Iio, S. Tadakuma, R. Haraduka, Y. Kanagawa, T. Imamura, M. Furue, on behalf of the Study Group for Yusho

引用次数: 7