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【medical-news】肝脏再生过程中的关键性受体被发
Description：In studies in mouse models, researchers at the University of California, San Diego (UCSD) School of Medicine have found that a cellular receptor involved in triggering cell death is also a necessary component of tissue repair and regeneration immediately following liver injury.
This discovery could have implications for early intervention or therapy in liver disease such as cirrhosis or hepatitis.
In a report to be published in the March 30 issue of the journal Science, Katerina Akassoglou, Ph.D. assistant professor in UCSD’s Department of Pharmacology, and colleagues describe the mechanism by which cells associated with liver damage, called hepatic stellate cells (HSCs), are activated by a cell surface molecule called the p75 neurotrophin receptor (p75NTR) to promote repair in the liver.
“Many therapeutics for liver disease target HSCs in order to kill them, but our study in animal models found that their initial activity could actually be protective,” said Akassoglou.
When chronic liver injury occurs, cells in the liver begin producing collagen and other proteins that lead to the formation of fibrous tissue and scarring. Akassoglou’s team looked at the molecular-cellular interface to discover how tissues respond to deposition of the fibrous protein, fibrin. In studies of a mouse model with excessive fibrin deposition in the liver, the researchers found that p75NTR signaling promotes the initial activation of HSC, which stimulates the proliferation of new hepatic cells to replace those that have been damaged. The effects of p75NTR at late stages of HSC activation and liver disease remain to be determined.
“We were intrigued by the increase of p75NTR expression after liver injury and hypothesized that p75NTR might regulate the progression of liver disease,” said Akassoglou. “By identifying p75NTR as the specific molecular link between HSCs and liver regeneration, p75NTR could provide a new therapeutic target for promoting cell regeneration and repair during chronic liver disease or injury.”
This discovery suggests the importance of sustaining p75 and early HSC activation – for example, in the case of liver transplantation when regeneration of liver cells is critical.
Additional contributors to the paper are first author Melissa A. Passino, Ryan A. Adams and Shoana L. Sikorski of the UCSD Department of Pharmacology. The research was supported by a grant from the National Institutes of Health/National Institute of Neurological Disorders and Stroke.
编译格式如下：
1.题目
2.第一段：研究者单位、研究者名字、期刊来源及卷数页码、研究结论
3.第二段：研究背景简介（如果没有，可略）、方法（样本数、研究手段）、研究具体结果，结论。
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本稿件为《医师报》约稿，署名统一为“丁香”，稿酬按照医师报标准发放 本人已认领该文编译，48小时后若未提交译文，请其他战友自由认领。 Researchers Identify Critical Receptor in Liver Regeneration
研究人员发现肝脏再生中的关键受体
Description：In studies in mouse models, researchers at the University of California, San Diego (UCSD) School of Medicine have found that a cellular receptor involved in triggering cell death is also a necessary component of tissue repair and regeneration immediately following liver injury.
概述：美国加州大学圣地亚哥 (UCSD)医学院的研究人员在使用小鼠模型进行研究中发现，一种与触发细胞损害相关的受体同时也是组织修复及肝脏损伤后立即再生所必需的因子。
This discovery could have implications for early intervention or therapy in liver disease such as cirrhosis or hepatitis.
这项发现对肝病（如肝硬化或肝炎）的早期干预或治疗具有一定意义。
In a report to be published in the March 30 issue of the journal Science, Katerina Akassoglou, Ph.D. assistant professor in UCSD’s Department of Pharmacology, and colleagues describe the mechanism by which cells associated with liver damage, called hepatic stellate cells (HSCs), are activated by a cell surface molecule called the p75 neurotrophin receptor (p75NTR) to promote repair in the liver.
在《科学》杂志3月30日刊的一篇论文中，加州大学圣地亚哥医学院药理系助教授Katerina Akassoglou博士及其同事描述到：这种机制是通过被称为P75神经营养因子受体(p75NTR)的细胞表面分子激活肝星形细胞(HSCs) （一种与肝细胞损害相关的细胞），继而促进肝脏修复。
“Many therapeutics for liver disease target HSCs in order to kill them, but our study in animal models found that their initial activity could actually be protective,” said Akassoglou.
“许多肝病的治疗都是靶向作用于HSCs，并杀灭它们，但是我们在对小鼠模型的研究中发现HSCs初期激活实际上是具有保护作用的，”Akassoglou说。
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作者:admin@医学,生命科学 2010-12-20 17:11
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