專題演講活動
題 目:CCRL2 is prostate cancer cell stemness mediator that regulates the organ-specific cancer metastasis
講 者:宋賢穎 副教授
講者單位:轉譯醫學博士學位學程
日 期:2021 年 8 月 16日
主辦單位:細胞治療與再生醫學研究中心
題 目:CCRL2 is prostate cancer cell stemness mediator that regulates the organ-specific cancer metastasis
講 者:宋賢穎 副教授
講者單位:轉譯醫學博士學位學程
日 期:2021 年 8 月 16日
主辦單位:細胞治療與再生醫學研究中心
敬邀參加109年12月16日(W3) 轉譯學程專家演講
主講人:王志豪 助理教授
講 題:CRISPR engineered human brown like adipocytes ameliorate metabolic dysregulation in mice
時 間:109年12月16日(W3) 13:00~15:00
地 點:大安校區 B2 B203會議室
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誠摯邀請本校教師與同仁們撥冗參與!
Special Lecture
Speaker: Chih-Hao Wang (Assistant Professor)
Date :2020-12-16 (Wednesday)
Venue: B203, B2F, Daan campus
Time:13:00~15:00
Language:English
CRISPR-engineered human brown-like adipocytes ameliorate metabolic dysregulation in mice
Abstract
Brown and white fats play crucial roles in systemic energy homeostasis. Brown fat is specific for energy dissipation and has multilocular lipid droplets, while white fat is the main site for storing excess fuel containing unilocular lipid droplets. The activity and amount of brown fat are inversely correlated with body mass index in mammals, making brown fat an appealing target for anti-obesity therapies. Aiming for transforming white fat to brown fat may hold great potential in preventing or treating obesity and obesity-related metabolic disorders, since white fat is more easily reachable and manipulatable considering its abundance and location. Uncoupling protein 1 (UCP1) is uniquely expressed in brown adipocytes and facilitates fuel utilization and energy expenditure. Here, we utilized the CRISPR/Cas9 synergistic activation mediator and specific gRNAs to boost endogenous UCP1 expression in human white adipocytes. The CRISPR/Cas9 engineered human brown fat-like (HUMBLE) cells had acquired human brown fat features when comparing bona fide human brown adipocytes derived from the same individual. Obese mice that received HUMBLE cell transplants showed lower body weight, a sustained improvement in glucose tolerance and insulin sensitivity, as well as increased energy expenditure. Mechanistically, increased arginine/nitric oxide (NO) metabolism in HUMBLE adipocytes promoted the production of NO that was carried by S-nitrosothiols and nitrite in red blood cells to activate endogenous brown fat and improved glucose homeostasis in recipient animals. Taken together, these data demonstrate the utility of using CRISPR/Cas9 technology to engineer human white adipocytes to display brown fat-like phenotypes and may open up cell-based therapeutic opportunities to combat obesity and diabetes.
Speaker: Prof. Kang-Yun Lee
Date :2020-12-9 (Wednesday)
Venue: B203, B2F, Daan campus
Time:13:00~15:00
Research Interests:
Epigenetic regulation of inflammation in airway disease
Cancer Immunology
Tumor microenvironment
From aberrant inflammation to repair and regeneration
– An Evolutionary Perspective on COPD
COPD has great impact on human health, which is the fourth leading cause of death worldwide. It is believed that chronic inflammation is central to the pathogenesis of the disease, causing progressive and irreversible airflow limitation. The inflammation in the airways and the lung is chronic, amplified and self-perpetuated with poor response to glucocorticoids. Although large efforts have been made to develop anti-inflammatory medications, particularly kinases inhibitors, none of them has promising results. Other directions including the epigenetic, anti-oxidant, specific immune abnormality (e.g. Th-17, Tc1, ILC1…) are still struggling. In addition to inflammation, other pathogenetic mechanisms might also have implication, in particular repair and regeneration. We currently focus on air pollution-induced emphysema and has identified novel players in the pathogenesis of the disease, such as Inter-alpha-trypsin inhibitor heavy chain H4 (ITIH4). In this talk, the evolution of the concept of COPD pathogenesis will be reviewed, which will point to a new direction of treatment of COPD.
唐獎教育基金會舉辦唐獎第四屆大師論壇–生醫場之會議影片已上傳,提供影片連結如下。歡迎踴躍觀看! English Version : https://www.youtube.com/watch?v=IqLpyTC7fbM&feature= youtu.be
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