Vinken Mathieu
Mathieu Vinken, Department of Toxicology, Faculty of Medicine and Pharmacy, Vrije Universiteit Brussel, Laarbeeklaan 103, B-1090 Brussels, Belgium.
World J Gastrointest Pathophysiol. 2011 Oct 15;2(5):82-7. doi: 10.4291/wjgp.v2.i5.82.
Direct intercellular communication mediated by gap junctions constitutes a major regulatory platform in the control of hepatic homeostasis. Hepatocellular gap junctions are composed of two hemichannels of adjacent cells which are built up by connexin proteins,in casu Cx32. Mathieu Vinken, Pofessor at the Department of Toxicology of the Free University Brussels-Belgium, was one of the first investigators to demonstrate that hepatic connexin expression is controlled by epigenetic mechanisms. In particular, he found that inhibitors of histone deacetylase enzymes enhance Cx32 production and gap junction activity in cultures of primary hepatocytes, a finding that is of importance for liver-based in vitro modelling. Professor Dr. Mathieu Vinken's recent work is focussed on the elucidation of the role of connexin proteins and their channels in the hepatocyte life cycle. Specific attention is paid to apoptosis in this context, whereby it has been found that Cx32 hemichannels control the termination of induced cell death in cultures of primary hepatocytes. Overall, Professor Dr. Mathieu Vinken's research can be considered as an important contribution to the field of hepatic connexin physiology.
由间隙连接介导的直接细胞间通讯构成了肝脏内稳态控制中的一个主要调节平台。肝细胞间隙连接由相邻细胞的两个半通道组成，这些半通道由连接蛋白构成，具体而言是Cx32。比利时布鲁塞尔自由大学毒理学系教授马蒂厄·温肯是最早证明肝脏连接蛋白表达受表观遗传机制控制的研究人员之一。特别是，他发现组蛋白脱乙酰酶抑制剂可增强原代肝细胞培养物中Cx32的产生和间隙连接活性，这一发现对于基于肝脏的体外模型构建具有重要意义。马蒂厄·温肯博士教授最近的工作集中在阐明连接蛋白及其通道在肝细胞生命周期中的作用。在这种情况下，特别关注细胞凋亡，结果发现Cx32半通道控制原代肝细胞培养物中诱导性细胞死亡的终止。总体而言，马蒂厄·温肯博士教授的研究可被视为对肝脏连接蛋白生理学领域的一项重要贡献。
