Damage of eukaryotic cells by the pore-forming toxin sticholysin II: Consequences of the potassium efflux

被引:36
|
作者
Cabezas, Sheila [1 ]
Ho, Sylvia [2 ]
Ros, Uris [1 ,3 ]
Lanio, Maria E. [1 ]
Alvarez, Carlos [1 ]
van der Goot, F. Gisou [2 ]
机构
[1] Univ Havana, Fac Biol, Ctr Prot Studies, St 25 455, Havana 10400, Cuba
[2] Ecole Polytech Fed Lausanne, Global Hlth Inst, Fac Life Sci, Stn 15, CH-1015 Lausanne, Switzerland
[3] Univ Tubingen, Interfak Inst Biochem, Hoppe Seyler Str 4, D-72076 Tubingen, Germany
来源
关键词
Pore-forming toxins; Cell damage; Potassium efflux; Sticholysin; Membrane recovery; ACTIVATED PROTEIN-KINASE; ANEMONE ACTINIA-EQUINA; PLASMA-MEMBRANE-REPAIR; ALPHA-TOXIN; STICHODACTYLA-HELIANTHUS; HEMOLYTIC-ACTIVITY; CYTOCIDAL ACTION; STRUCTURAL BASIS; N-TERMINUS; CYTOLYSIN;
D O I
10.1016/j.bbamem.2017.02.001
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Pore-forming toxins (PFTs) form holes in membranes causing one of the most catastrophic damages to a target cell. Target organisms have evolved a regulated response against PFTs damage including cell membrane repair. This ability of cells strongly depends on the toxin concentration and the properties of the pores. It has been hypothesized that there is an inverse correlation between the size of the pores and the time required to repair the membrane, which has been for long a non-intuitive concept and far to be completely understood. Moreover, there is a lack of information about how cells react to the injury triggered by eukaryotic PFTs. Here, we investigated some molecular events related with eukaryotic cells response against the membrane damage caused by sticholysin II (all), a eukaryotic PFT produced by a sea anemone. We evaluated the change in the cytoplasmic potassium, identified the main MAPK pathways activated after pore-formation by Stll, and compared its effect with those from two well-studied bacterial PFTs: aerolysin and listeriolysin O (LLO). Strikingly, we found that membrane recovery upon all damage takes place in a time scale similar to LLO in spite of the fact that they form pores by far different in size. Furthermore, our data support a common role of the potassium ion, as well as MAPKs in the mechanism that cells use to cope with these toxins injury. (C) 2017 Elsevier B.V. All rights reserved.
引用
收藏
页码:982 / 992
页数:11
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