Cholesterol stimulates and ceramide inhibits Sticholysin II-induced pore formation in complex bilayer membranes

A1 Journal article (refereed)

Internal Authors/Editors

Publication Details

List of Authors: Ida Alm, Sara García-Linares, José G. Gavilanes, Álvaro Martínez-del-Pozo, J Peter Slotte
Publisher: Elsevier
Publication year: 2015
Journal: BBA - Biomembranes
Volume number: 1848
Issue number: 4
Start page: 925
End page: 931
eISSN: 1879-2642


The pore forming capacity of Sticholysin II (StnII; isolated from Stichodactyla helianthus) in bilayer membranes
containing 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC), palmitoylsphingomyelin (PSM) and either
cholesterol or palmitoyl ceramide (PCer) has been examined. The aim of the study was to elucidate how
the presence of differently ordered PSM domains affected StnII oligomerization and pore formation. Cholesterol
is known to enhance pore formation by StnII, and our results confirmed this and provide kinetic information for
the process. The effect of cholesterol on bilayer permeabilization kinetics was concentration-dependent. In the
concentration regime used (2.5–10 nmol cholesterol in POPC:PSM 80:20 by nmol), cholesterol also increased
the acyl chain order in the fluid PSM domain and thus decreased bilayer fluidity, suggesting that fluidity per se
was not responsible for cholesterol's effect. Addition of PCer (2.5–10 nmol) to the POPC:PSM (80:20 by nmol) bilayers
attenuated StnII-induced pore formation, again in a concentration-dependent fashion. This addition also
led to the formation of a PCer-rich gel phase. Addition of cholesterol to PCer-containingmembranes could partially
reduce the inhibitory effect of PCer on StnII pore formation.We conclude that the physical state of PSM(as influenced
by either cholesterol or PCer) affected StnII binding and pore formation under the conditions examined.

Last updated on 2020-09-08 at 04:59