Second International Symposium-Epigenetic Regulation of Skin Regeneration and Aging: From Chromatin Biology towards the Understanding of Epigenetic Basis of Skin Diseases.
Second International Symposium-Epigenetic Regulation of Skin Regeneration and Aging: From Chromatin Biology towards the Understanding of Epigenetic Basis of Skin Diseases.
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DOI：
10.1016/j.jid.2017.01.037
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发表时间：
2017-08
期刊：
影响因子：
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通讯作者：
V. Botchkarev
中科院分区：
文献类型：
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作者：
V. Botchkarev
自2012年在英国布拉德福德大学召开第一届皮肤表观遗传学国际研讨会(Botchkarev等人，2013)以来，该领域的研究取得了实质性进展，有助于理解表观遗传调控机制如何与信号通路和转录因子协同工作来控制正常皮肤的基因表达，以及表观遗传机制如何在包括炎症性皮肤病和癌症在内的许多病理条件下失控。为了总结皮肤表观遗传学的最新成就，并为研究人员提供机会再次会面并讨论这一迅速扩大的领域的最重要方面，2016年3月17-19日在英国布拉德福德大学皮肤科学中心举行了国际研讨会“皮肤再生和衰老的表观遗传学调控”。来自欧洲、中国、日本、新加坡和美国的学术机构以及制药和个人护理行业的110多名代表出席了研讨会。研讨会包括8场主题演讲、John M.Wood纪念讲座和27场分成6节的演讲。在开幕式上，南加州大学洛杉矶分校的庄正明教授和英国伦敦国王学院的Fiona Watt教授介绍了皮肤是表观遗传学研究的优秀模型，加州大学旧金山分校的Terumi Kohwi-Shigematsu教授介绍了表观遗传机制如何促进肿瘤细胞转化的数据。在之前关于DNA甲基转移酶1在控制小鼠毛囊发育和衰老中的作用的研究(Li等人，2012)之后，Chuong描述了角蛋白基因在鸡基因组中的组织方式。与哺乳动物类似，鸡角蛋白基因在第25和27号染色体上聚集在不同的基因座上；而第25号染色体上的β-角蛋白基因在表达上表现出更多的附件间差异，而第27号染色体上的那些基因表现出更多的附件内差异，从而为表观遗传调控研究提供了特定的分子靶点(Wu等人，2015年)。Watt在最近发现的涉及不同表观遗传调控因子的相互作用网络的背景下描述了信号和表观遗传机制之间的相互作用，该网络影响了涉及表皮干细胞锚定到其利基的两个功能相关的基因集(Mulder等人，2012年)。Kohwi-Shigematsu讨论了染色质结构蛋白和基因组组织者SATB1如何通过调控不同细胞类型癌症中的高阶染色质重组和表观遗传修饰来调节基因来改变其表型，以调控表观遗传修饰、转录和驱动转移(Kohwi-Shigematsu等人，2012，Kohwi-Shigematsu等人，2013)。
After the First International Symposium on Skin Epigenetics at the University of Bradford (UK) in 2012 (Botchkarev et al., 2013), the research in this area has progressed substantially toward understanding how epigenetic regulatory machinery operates in concert with signaling pathways and transcription factors to control gene expression in normal skin and how epigenetic mechanisms are dysregulated in many pathological conditions including inflammatory skin disorders and cancer. To summarize recent achievements in skin epigenetics and to provide an opportunity for investigators to meet again and discuss the most important aspects of this rapidly expanding area, International Symposium “Epigenetic Regulation of Skin Regeneration and Aging” was held on March 17–19, 2016, in the Centre for Skin Sciences at the University of Bradford, UK. The Symposium was attended by over 110 participants from Europe, China, Japan, Singapore, and the United States, representing academic institutions as well as pharmaceutical and personal care industries. The Symposium program included eight Keynote lectures, the John M. Wood Memorial Lecture, and 27 talks organized into six sessions.In the Opening lectures, Prof. Cheng-Ming Chuong (University of Southern California, Los Angeles) and Prof. Fiona Watt (King’s College London, UK) introduced skin as an excellent model for epigenetic research, and Prof. Terumi Kohwi-Shigematsu (University of California, San Francisco) presented data on how epigenetic machinery contributes to neoplastic cell transformation. Following up the previous research on the role of DNA methyltransferase 1 in the control of hair follicle development and aging of mice (Li et al., 2012), Chuong described about how keratin genes are organized in the chicken genome. Similar to mammals, chicken keratin genes are clustered into distinct loci on chromosomes 25 and 27; whereas β-keratin genes on chromosome 25 show more inter-appendage differences in their expression, those on chromosome 27 show more intra-appendage differences, thus providing specific molecular targets for the study of epigenetic regulation (Wu et al., 2015). Watt described interplay between signaling and epigenetic mechanisms in the context of a recently discovered network of interactions involving different epigenetic regulators that affects two functionally related gene sets involved in the anchorage of epidermal stem cells to their niches (Mulder et al., 2012). Kohwi-Shigematsu discussed how the chromatin architectural protein and genome organizer SATB1 enables cells to change their phenotypes by regulating genes through higher-order chromatin reorganization and epigenetic modification in cancers of distinct cell types to regulate epigenetic modification, transcription, and drive metastasis (Kohwi-Shigematsu et al., 2012, Kohwi-Shigematsu et al., 2013).