Intracellular Ca(2+) operates a switch between repair and lysis of streptolysin O-perforated cells

Babiychuk, E B; Monastyrskaya, K; Potez, S; Draeger, A (2009). Intracellular Ca(2+) operates a switch between repair and lysis of streptolysin O-perforated cells. Cell death and differentiation, 16(8), pp. 1126-34. Basingstoke: Nature Publishing Group 10.1038/cdd.2009.30

Full text not available from this repository. (Request a copy)

Pore-forming (poly)peptides originating from invading pathogens cause plasma membrane damage in target cells, with consequences as diverse as proliferation or cell death. However, the factors that define the outcome remain unknown. We show that in cells maintaining an intracellular Ca(2+) concentration [Ca(2+)](i) below a critical threshold of 10 microM, repair mechanisms seal off 'hot spots' of Ca(2+) entry and shed them in the form of microparticles, leading to [Ca(2+)](i) reduction and cell recovery. Cells that are capable of preventing an elevation of [Ca(2+)](i) above the critical concentration, yet are unable to complete plasma membrane repair, enter a prolonged phase of [Ca(2+)](i) oscillations, accompanied by a continuous shedding of microparticles. When [Ca(2+)](i) exceeds the critical concentration, an irreversible formation of ceramide platforms within the plasma membrane and their internalisation drives the dying cells beyond the 'point of no return'. These findings show that the extent of [Ca(2+)](i) elevation determines the fate of targeted cells and establishes how different Ca(2+)-dependent mechanisms facilitate either cell survival or death.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Pre-clinic Human Medicine > Institute of Anatomy > Cell Biology

UniBE Contributor:

Babiychuk, Eduard and Potez, Sarah

ISSN:

1350-9047

Publisher:

Nature Publishing Group

Language:

English

Submitter:

Factscience Import

Date Deposited:

04 Oct 2013 15:11

Last Modified:

04 May 2014 23:22

Publisher DOI:

10.1038/cdd.2009.30

PubMed ID:

19325569

Web of Science ID:

000267948900007

URI:

https://boris.unibe.ch/id/eprint/31090 (FactScience: 195494)

Actions (login required)

Edit item Edit item
Provide Feedback