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Antimicrobial and immunostimulatory peptide, KLK, induces an increase in cytosolic Ca 2+ concentration by mobilizing Ca 2+ from intracellular stores
Author(s) -
Weghuber Julian,
Lipp Anna M.,
Stadlbauer Jacqueline,
Aichinger Michael C.,
Ruprecht Verena,
Sonnleitner Alois,
Schütz Gerhard J.,
Henics Tamás
Publication year - 2010
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20100408
Subject(s) - intracellular , cytosol , peptide , phosphatidylserine , chemistry , biophysics , microbiology and biotechnology , membrane , biochemistry , apoptosis , biology , phospholipid , enzyme
The cationic antimicrobial immunomodulatory peptide, KLK (KLKL 5 KLK), exerts profound membrane interacting properties, impacting on ultrastructure and fluidity. KLK–membrane interactions that lead to these alterations require the ability of the peptide to move into an α‐helical conformation. We show that KLK induces an increase of the intracellular Ca 2+ concentration in human T24 cells. The effect of KLK is buffer‐sensitive, as it is detected when HBSS buffer is used, but not with PBS. This, together with the lack of effect of the middle leucine‐to‐proline‐substituted peptide derivative [KPK (KLKLLPLLKLK)], indicates that it is the conformational propensity rather than the net positive charge that contributes to the effect of KLK on intracellular Ca 2+ level of T24 cells. We show that, although KLK slightly stimulates Ca 2+ influx into the cell, the bulk increase of Ca 2+ levels is due to KLK‐induced depletion of intracellular Ca 2+ stores. Finally, we demonstrate a KLK‐induced switch of PS (phosphatidylserine) from the inner to the outer plasma membrane leaflet that contributes to the onset of early apoptotic changes in these cells.